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Saudi Journal of Kidney Diseases and Transplantation
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Year : 1999  |  Volume : 10  |  Issue : 3  |  Page : 286-297
Effect of Age on Hypertension: Analysis of Over 4,800 Referred Hypertensive Patients


Department of Medicine, SUNY Health Science Center, Syracuse, New York, Slocum-Dickson Medical Group, New Hartford, New York, USA

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   Abstract 

We evaluate in this study the factors associated with the effect of age on blood pressure in more than 4800 patients. Their physicians referred them to evaluate for secondary causes for their hypertension. Factors studied included history and physical examination, serum sodium, potassium and creatinine, a stimulated plasma renin and catecholamine. We also studied the blood pressure response to infusion of either saralasin (an angiotensin II analogue) or enalapril (an angiotensin converting enzyme inhibitor), and plasma aldosterone and cortisol after infusion of saline. We measured serum thyroxin and thyroid stimulating hormone concentrations on 1061 consecutive patients in this series. The results of our study show that increased age is associated with a significant increase in the prevalence of hypertension and especially of systolic hypertension after age 60 years. Increased obesity between age 30-50 years is associated with significant increases in diastolic blood pressure and this trend is also seen in African-Americans who are heavier than whites. Increased age is associated with an increased prevalence of secondary forms of hypertension including atherosclerotic renovascular hypertension, renal insufficiency and primary hypothyroidism.

Keywords: Hypertension, Age, Elderly, Secondary causes, Systolic blood pressure, Obesity.

How to cite this article:
Anderson GH. Effect of Age on Hypertension: Analysis of Over 4,800 Referred Hypertensive Patients. Saudi J Kidney Dis Transpl 1999;10:286-97

How to cite this URL:
Anderson GH. Effect of Age on Hypertension: Analysis of Over 4,800 Referred Hypertensive Patients. Saudi J Kidney Dis Transpl [serial online] 1999 [cited 2019 May 22];10:286-97. Available from: http://www.sjkdt.org/text.asp?1999/10/3/286/37237

   Introduction Top


With age, there is an increase in blood pressure in the general population as well as in people with hypertension. We analyze in this study the data of more than 4800 patients, in order to study the relationship of the increase in blood pressure with age and the involved factor.

Factors studied included history and phy­sical examination, serum sodium, potas­sium and creatinine, a stimulated plasma renin and catecholamine. We also studied the blood pressure response to infusion of either saralasin (an angiotensin II analogue) or enalapril (an angiotensin converting enzyme inhibitor), and plasma aldosterone and cortisol after infusion of saline.


   Methods Top


We studied more than 4800 hypertensive patients, referred by their physicians for evaluation of possible secondary causes for their hypertension. Previous attempts to control their hypertension were considered, by their referring physicians, to have been unsatisfactory. When hypertension was mild or moderately severe, antihypertensive medications were progressively reduced and stopped one week or more before investiga­tions. Patient with severe hypertension were studied on the day of stopping their anti­hypertensive drugs, or were admitted for progressive reduction and cessation of these drugs 2-3 days before the studies.

Initially, after reading and signing a consent document the patients had their blood pressure measured in both arms while reclining on a hospital bed and in one arm after standing for 2-3 min. A trained nurse, using a standard mercury sphygmomanometer measured blood pressure. An indwelling intravenous needle was then inserted into a forearm vein and blood was drawn for measurement of serum electrolytes, creatinine, and thyroxin and thyroid stimulation hormone concentrations. Furosemide (40 mg) was then injected intravenously and the patients remained recumbent from 0800 to 0900 h, while a hypertension-related history was obtained and a physical examination was performed. Thus, and by using the referring physician's data, evidence was obtained for the presence of vascular disease (heart, cerebrovascular or peripheral), and patients were categorized by the presence or absence of atherosclerosis. The subjects then stood and walked about for one hour, at the end of which blood was drawn from all patients for measurement of plasma renin activity (PRA) [1], and aldosterone and catecholamine concentrations [2] Blood pressure was then measured every minute for 30-40 min with the patients recumbent, using an Arteriosonde or Dinamap (Critikon; Johnson and Johnson, Tampa, Florida, USA), after which another blood sample was withdrawn through the indwelling needle for measurements of plasma catecholamine concentrations. The blood pressure response was then observed during intravenous infusion of either the angiotensin II antagonist saralasin at increasing rates [3] or (in the last 100 patients) enalapril at 20 mg over 20 min. After these measurements lunch was served and an intravenous infusion of 0.9% saline solution (2 liters) was administered over a 3 to 4 hour period, at the end of which blood was drawn from all patients, recumbent, for plasma aldosterone and cortisol measurements. Depending on the results of these studies, additional measurements were made on another day, to establish the presence of secondary hypertension.

Renovascular stenosis was strongly suggested by a fall in blood pressure of > 10/7 mmHg during the saralasin [3] or enalapril infusion. Patients were designated as having renovascular hypertension if they met any of the following criteria: renal angiogram showing at least a 75% narrowing of one or both renal arteries; a ratio of PRA in the renal veins of at least 1.5, together with a renal isotope scan showing a decreased flow in the kidney with the highest venous PRA; renal angiogram showing unilateral narrowing of < 75% but renal vein renins lateralizing to that side; a fall in blood pressure to < 140/90 mmHg one month after a renal angioplasty or surgical procedure (bypass or nephrectomy); or renal artery narrowing of > 75% determined at autopsy. There were 126 such patients determined to have atherosclerotic renal arterial stenosis and 23 to have fibromuscular stenosis by typical angiographic appearances.

The angiographic evidence that athero­sclerosis was causing the renal arterial stenosis in patients by the second and third of these criteria was supported by the age of these patients (usually >45 years) and evidence of atherosclerosis elsewhere (atherosclerotic heart disease, intermittent claudication or presence of bruits).

Patients who had a serum creatinine concentration of > 176 µmol/1 (> 2.0 mg/dl) were designated as having renal insufficiency. Renal insufficiency, whether it is the cause of, or the result of hypertension, usually causes sodium retention, and in this way causes hypertension or secondarily aggravates preexisting hypertension.

Serum thyroxin and thyroid stimulating hormone concentrations were measured on 1061 consecutive patients in this series, and patients were deemed to have hypothyroidism (primary) if their thyroid stimulating hormone level was above the upper limit of the normal range (> 70 µU/ml). That hypothyroidism can actually cause hypertension was shown previously in 32% of a group of hypothyroid patients who had high blood pressures, and whose diastolic blood pressure fell to < 90 mmHg during replacement therapy with thyroxine, with eventual withdrawal of all anti­hypertensive drugs. [4] The projected number of patients with primary hypothyroidism in the 4429 patients presented below in [Table - 2] was extrapolated from the above 1061 patients.

As described previously, patients were determined to have Cushing's syndrome,[5] primary aldosteronism [6] or pheochromo­cytoma [7] by appropriate confirmatory measurements after the initial screening. A normal plasma renin activity was taken as 1.7-8.5 ng/ml per hour and a normal plasma aldosterone after infusion of two liters isotonic saline was < 8.5 ng%. All patients with abnormal suppressed plasma aldosterone were confirmed to have primary aldosteronism by a 3-day suppression test with high salt and fluorohyrocortisone or deoxy­corticosterone acetate, as described previously. [6] All patients with primary aldosteronism had computed tomography scans of the adrenal glands and, in most cases, adrenal vein catheterization to determine the type of hyperaldosteronism.


   Statistical analysis Top


We used the means to report the values in each group. We used Chi-square and analysis of variance (ANOVA) in the comparisons among the subgroups. We set the level of significance to P≤O.05.


   Results Top


In [Table - 1] is shown the characteristics of the population group being studied. Sixty five percent of the patients were receiving blood pressure medications but 68.7% were off all blood pressure medications for at least one week. At ages 18-29 years 83% of the patients were off medications for > one week but over age 70 only 45% of them were to discontinue their medications for > one week (p < 0.000001).

In [Table - 2] is listed the percentages (numbers) of the different types of secondary hypertension in each age group from 18 to > 70 years. Also listed is the percentage (total number) for each group. There was an increase with age in the prevalence of renovascular hypertension, renal insufficiency and primary hypothyroidism. In patients aged > 70 years the prevalence of secondary forms of hypertension was 17.4%. Primary aldosteronism due to bilateral adrenocortical hyperplasia was relatively uncommon above 60 years of age, whereas primary aldosteronism due to an adenoma was evenly distributed by age.

For the secondary hypertensive group as a whole, compared with the essential hypertensives, there were significantly higher: mean age (P≤O.001), systolic blood pressure (P≤O.001), diastolic blood pressure (P≤0.001), serum creatinine concentration (P≤0.001); and significantly lower Quetelet index (PO.01) and serum potassium concentration (P≤O.05).

The mean age of patients with essential hypertension was significantly lower than that of patients with atherosclerotic renovascular hypertension (P≤0.001), primary aldosteronism due to adenoma (P≤0.05) or bilateral hyperplasia (P≤0.05), pheochromocytoma (P≤O.05), primary hypothyroidism (P≤O.001) or renal insufficiency (P≤O.01). On the other hand, the mean age of patients with essential hypertension was significantly higher than the mean age of patients with fibromuscular stenosis and renovas, cular hypertension (P≤O.001).

Compared with findings in patients with essential hypertension, there were significantly higher percentages of woman than men with fibromuscular renovascular hypertension (P≤O.008), Cushing's syndrome (P≤O.007) or primary hypothyroidism (P≤O.0001), and significantly more men than women with renal insufficiency (P≤O.030).

Compared with the essential hyperten­sives, there were significantly fewer African-American patients than White Americans with atherosclerotic renovascular hypertension (P≤O.00001) or primary hypothyroidism (PO.020), and significantly more of them with primary aldosteronism due to bilateral hyperplasia (P≤O.0001) or with renal insufficiency (P≤O.0024).

Compared with the essential hypertensives, the mean systolic blood pressure was significantly higher in patients with atherosclerotic renovascular hypertension (P ≤ 0.001), primary aldosteronism due to adenoma and hyperplasia (both P≤O.001), or renal insufficiency (P≤O.001).

Compared with the essential hyperten­sives, the mean diastolic blood pressure was significantly higher for patients with athero­sclerotic and fibromuscular renovascular hypertension (both P≤O.001), primary aldosteronism due to adenoma and hyper­plasia (both P≤O.001), or renal insufficiency (P≤O.001).

Compared with the essential hypertensives, the Quetelet index was significantly lower for patients with fibromuscular (P≤O.001), atherosclerotic (P≤O.01) renovascular hypertension, pheochromocytoma (PO.05) or renal insufficiency (P≤O.01). The same index was significantly higher for patients with primary aldosteronism due to hyperplasia (P≤O.01).

Patients with atherosclerotic renovascular hypertension had significantly (P≤O.01) higher serum creatinine concentrations than patients with essential hypertension. Patients with essential hypertension had a significantly higher serum potassium con­centration than patients with atherosclerotic renovascular hypertension (P≤0.05), and primary aldosteronism due to adenoma (P≤O.001), and hyperplasia (P≤O.001).

Patients with initial evidence of atherosclerosis had a significantly (P≤0.001) higher prevalence of atherosclerotic renovascular hypertension (9.5%) or renal insufficiency (8.0%) than those without atherosclerosis. Overall, 23.4% of patients with atherosclerosis had evidence of a possible secondary cause for their hypertension.

The effect of increasing age on the prevalence of selected forms of secondary hypertension was analyzed. There was a significant (PO.000001) increase in the relative prevalence of secondary forms of hypertension with age. By age > 70 years the prevalence rate was over 3.5-fold that for age 18-29 years. This increase was accounted for entirely by the increased prevalence rates for renovascular hypertension, hypothyroidism and renal insufficiency.

[Table - 3] shows the effect of age on measured parameters for patients with essential hypertension. There was a significant increase in systolic blood pressure with age. There was also a significant increase in diastolic blood pressure with age, however, it decreased after age 60 years.

The pulse did not change and the Quetelet index significantly increased with age and then decreased after age 60 years. The calculated creatinine clearance [8] significantly decreased with age.

Additional parameters related to age for patients with essential hypertension are listed in [Table - 4]. The plasma renin significantly decreased with age, while the stimulated plasma norepinephrine significantly increased with age as indicated in the table. These two parameters are reported for patients who have been off all blood pressure medications for at least one week or more. This table also shows a significant increase of prevalence of diabetes mellitus and cardiovascular complications with age.

Various parameters of patients with essential hypertension, grouped according to a measure of obesity, the Quetelet index, ranging from lean (<25), to heavy (25-29) or obese (>=30), are listed in [Table - 5]. The Quetelet index increased with age. This increase might have an effect upon blood pressure and other parameters. There was a significant increase in systolic and a slight but not significant increase in diastolic blood pressure with increased obesity. The calculated creatinine clearance increased with increased obesity as previously reported. [9] The lean group was the youngest and the obese group was younger than the heavy group.

In [Table - 6], plasma renin and norepine­phrine are presented only for those patients who have been off all blood pressure medi­cations for > one week. There was a significant decrease in plasma renin with increasing obesity. The plasma norepine-phrine showed a slight decrease with obesity. Obesity was also associated with a significant increase in the percentage of diabetes mellitus but not of cardiovascular complications.

Since the above results showed that increasing obesity could be associated with increased blood pressure, it was decided to plot the diastolic blood pressure in various age groups versus the Quetelet index in African-Americans and Whites. It was decided to separate the African-Americans, since the former, in our population, were heavier and had higher blood pressure than Whites. Results in [Figure - 1] show that there was a significant (p=0.0004) correlation between the two parameters for the two groups. Also shown is the mean and 95% confidence level for the plotted data. In the legend, the equation for this curve is given. For example, a change in weight of 10 Kg (22.2 lbs. or Quetelet of 3.3 kg/m2) is associated with a change in diastolic blood pressure of 10 mmHg. In both groups, the diastolic blood pressure was lowest in the youngest group, increased to a maximum at age 40-59 years and then declined after that. It is also apparent that the increased diastolic blood pressure in African-Americans was significantly associated with increasing obesity, suggesting but not proving a cause and effect. It should also be noted that the analysis of the same data for patients off all blood pressure medication for > one week showed a significant correlation between the two parameters for both groups (p=0.0005). There was no significant correlation between the Quetelet index and the systolic blood pressure.

In [Figure - 2], we plotted the Quetelet index versus the diastolic blood pressure for those with essential hypertension in comparison with various forms of secondary hyperten­sion. It is apparent that compared to those with essential hypertension, those with some forms of secondary hypertension had a higher diastolic blood pressure than would be expected for their obesity. This is true for patients with primary aidosteronism due to adenoma, pheochromocytoma, renal insufficiency, atherosclerotic renovascular hypertension and especially renovascular hypertension due to fibromuscular hyperplasia

This suggests that factors other than obesity may play a major role in increasing the diastolic blood pressure (the rennin­angiotensin system, plasma aldosterone and catecholamines). On the other hand, the plots for those with primary aldosteronism due to hyperplasia and Cushing's syndrome were similar to those with essential hypertension suggesting that obesity may play an etiological role.

[Table - 7] summarizes the effect of age on various parameters in hypertensive patients.


   Discussion Top


Our results are consistent with the epidemiological data on the general popu­lation that systolic and diastolic blood pressure increase with age and that systolic blood pressure continues to increase after the seventh decade, while the diastolic blood pressure declines. Age significantly increases the prevalence of secondary forms of hypertension. This is especially true for patients with atherosclerotic renovascular hypertension, renal insufficiency and primary hypothyroidism.

As shown in our study, the plasma renin decreases with age as has been previously reported in both normotensive and hyper­tensive people. [10] In our study the plasma nore­pinephrine significantly increased with age but this could partially represent the normal increase in plasma norepinephrine with age and does not necessarily imply a cause for the increase in blood pressure with age. [11]

In our study, there was a significant increase in the prevalence of diabetes mellitus (type 2) in people with essential hyper­tension. Patients with essential hypertension have been reported to have insulin resistance that is independent of the level of obesity and which significantly correlated with the severity of the hypertension. [12] In pre-hypertensive individuals, it has been shown that high plasma insulin was associated with a two fold greater risk for hyper­tension eight years later. [13] A recent report in diabetic patients with hypertension showed that tight blood pressure control over 10 years significantly reduced cardio­vascular complications. [14] Thus the preva­lence of diabetes mellitus increases with age in patients with essential hypertension and the blood pressure in these patients should be more vigorously treated.

The well-known increase in serum cholesterol with age could certainly contribute to the increased prevalence of atherosclerotic renovascular hypertension as was shown in our study. Moreover, our study demonstrated an increase of hypothyroidism with age, which can result in hypertension in as much as 1/3 of these patients, as previously reported. [4]

The decrease in creatinine clearance with age could cause sodium retention and thus aggravate the presence of hypertension. [15] In fact, in our study, after the intravenous administration of furosemide the patients with renal insufficiency excreted signify­cantly less sodium than the patients without renal insufficiency.

It has been shown that the higher the level of diastolic blood pressure, the greater the prevalence of secondary forms of hyper­tension including renal insufficiency, primary aldosteronism and renovascular hypertension. [16] As shown in our study, a higher diastolic blood pressure in relationship to the obesity index suggests secondary causes of hypertension.

In our study, the decrease in the Quetelet index after age 60 could be due to heavier hypertensives having a higher mortality. However, our study demonstrated that obesity did not affect the prevalence of cardiovascular complications. This result is consistent with studies by Kannel et al [17] and Selmer et al [18] showing similar cardiovas­cular complication incidence rate in lean and obese individuals.

The decreased plasma renin activity with increased obesity has not been reported before. One possible cause would be the increased sodium retention associated with increased insulin levels found with obesity. [19] There was a slight decrease in the stimulated plasma norepinephrine with increased obesity, perhaps related to the obesity-augmented pressure sensitivity to norepinephrine.[20]

A meta-analysis in 1987 in hypertensive patients showed that weight loss by dietary intervention lowered blood pressure. [21] A 10-kg weight loss reduced systolic blood pressure by 7 mmHg and diastolic blood pressure by 3 mmHg. A study in older (age 60-80 years) hypertensive adults (Trial of Non-pharmacological Intervention in the Elderly, TONE) whose blood pressure medications were withdrawn showed that weight loss over 2 years reduced the recurrence of high blood pressure. [22] Results were similar for men and women, African­Americans and Whites. [23]

Results of our study suggest that the increase in diastolic blood pressure up to age 60 years is associated with an increased level of obesity, whether for African­Americans or Whites. They also suggest that African-Americans have a higher diastolic blood pressure than Whites in part because of their higher obesity. These results are consistent with a recent article relating increased prevalence of hypertension with obesity in seven populations of African-American origin. [24] Prevention of obesity could have a significant effect on the prevalence of hypertension as has been suggested before. [25]

Finally, though not included in our study, several recent studies have shown the benefit of treatment of hypertension in elderly people. The European Working Party on High Blood Pressure in the Elderly (EWPHE) trial showed that active treatment reduced cardiovascular mortality by 27%, fatal myocardial infarctions by 60% and strokes by 50%. [26] The Swedish Trial in Old Patients with Hypertension (STOP­Hypertension) showed that treatment for hypertensive patients age 70-84 significantly reduced stroke by 47% and total mortality by 73%. [27]

The Systolic Hypertension in the Elderly Program (SHEP) showed treatment of only systolic hypertension in the elderly (mean age =72 years) significantly reduced strokes by 37%, cardiovascular events by 32% and nonfatal myocardial infarctions by 33%. [28]

In summary, increased age is associated with a significant increase in the prevalence of hypertension and especially of systolic hypertension after age 60 years. Increased obesity between age 30-50 years is associated with significant increases in diastolic blood pressure and this trend is also seen in African-Americans who are heavier than Whites. Increased age is associated with an increased prevalence of secondary forms of hypertension including atherosclerotic renovascular hypertension, renal insufficiency and primary hypothyroidism. Vigorous treatment of essential hypertension in the elderly including those with systolic hype-tension and in patients with diabetes can significantly reduce cardiovascular complications.


   Acknowledgements Top


The author gratefully acknowledges the help of all nurses at the Clinical Research Center, and the technicians who performed the assays including T. Scullard, C. Jones, S. Brennan and K. Cusano.

Sponsorship: This study was supported by research grants (HL 26748 and AG 03055) from the National Institutes of Health, and by a Clinical Research Center Grant (RR229) from the Division of Research Facilities and Resources, US Public Health Service.

 
   References Top

1.Streeten DH, Freiberg JM, Anderson GH, Dalakos TG. Identification of angioten-sinogenic hypertension in man using 1-sar-8-ala angiotensin II (Saralasin, PI 13). CircRes 1975;36(Suppl l):125-32.  Back to cited text no. 1    
2.Streeten DH, Auchincloss JH Jr, Anderson GH Jr, Richardson RL, Thomas FD, Miller JW. Orthostatic hyper­tension. Patho-genetic studies. Hyper­tension 1985;7:196-203.  Back to cited text no. 2    
3.Streeten DHP, Anderson GH, Freilberg JM, Dalakos TG. Use of an angiotensin II antagonist (saralasin) in the recognition of "angiotensinogenic" hypertension. N Engl JMed 1975;292:657-62.  Back to cited text no. 3    
4.Streeten DP, Anderson GH Jr, Howland T, Chiang R, Smulyan H. Effects of thyroid function on blood pressure. Recognition of hypothyroid hypertension. Hypertension 1988;11:78-83.  Back to cited text no. 4    
5.Dalakos TG, Elias AN, Anderson GH Jr, Streeten DH, Schroeder ET. Evidence for an angiotensinogenic mechanism of the hypertension of Cushing's syndrome. J Clin Endocrinol Metab 1978;46:114-8.  Back to cited text no. 5  [PUBMED]  
6.Streeten DH, Tomycz N, Anderson GH. Reliability of screening methods for the diagnosis of primary aldo­steronism. Am J Med 1979;67:403-13.  Back to cited text no. 6  [PUBMED]  
7.Bravo EL, Gifford RW Jr. current concepts. Pheochromocytoma: diagnosis, localization, and management. N Engl J Med 1984;311: 1298-303.  Back to cited text no. 7    
8.Coyne DW. Evaluation of the patient with renal disease. In The Washington Manual of Medical Therapeutics. Edited by Carey CF, Lee HH and Woeltje KF. Lippincott-Raven 1998;p227.  Back to cited text no. 8    
9.Ribstein J, du Cailar G, Mimran A. Combined renal effects of overweight and hypertension. Hypertension 1995;26:610-5.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Helmer OM. Renin activity in blood from patients with hypertension. Can Med Assoc J 1964;90:221-25.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Goldstein DS, Lake CR. Plasma norepine-phrine and epinephrine levels in essential hypertension. Fed Proc 1984;57-61.  Back to cited text no. 11    
12.Ferrannini E, Buzzigoli G, Bonadonna R, et al. Insulin resistance in essential hypertension. N Engl J Med 1987;317:350-7.  Back to cited text no. 12  [PUBMED]  
13.Haffner SM, Ferrannini E, Hazuda HP, Stern MP. Clustering of cardiovascular risk factors in confirmed prehypertensive individuals. Hyper­tension 1992;20:38-45.  Back to cited text no. 13    
14.Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38. UK Prospective Diabetes Study Group. BMJ 1998;317:703-13.  Back to cited text no. 14  [PUBMED]  [FULLTEXT]
15.Brown MA, Whitworth JA. Hyper­tension in human renal disease. J Hypertens 1992; 10:701-12.  Back to cited text no. 15  [PUBMED]  
16.Anderson GH Jr, Blakeman N, Streeten DH. The effect of age on prevalence of secondary forms of hypertension in 4,429 consecutively referred patients. J Hypertens 1994;12:609-15.  Back to cited text no. 16  [PUBMED]  
17.Kannel WB, Zhang T, Garrison RJ. Is obesity related hypertension less of a cardiovascular risk? The Framingham Study. Am Heart J 1990;120:l 195-201.  Back to cited text no. 17    
18.Selmer R, Tyerdal A. Body mass index and cardiovascular mortality at different levels of blood pressure: a prospective study of Norwegian men and women. J Epidemiol Community Health 1995;49: 265-70.  Back to cited text no. 18    
19.Gupta AK, Clark RV, Kirchner KA. Effects of insulin on renal sodium excretion. Hypertension 1992;19(Suppl I): 178-82.  Back to cited text no. 19    
20.Baron AD, Brechtel G, Johnson A, et al. Interactions between insulin and norepine-phrine on blood pressure and insulin sensitivity. Studies in lean and obese men. J. Clin Invest 1994;93:2453-62.  Back to cited text no. 20    
21.McMahon S, Cutler J, Brittain E, Higgins M. Obesity and hypertension: epidemiological and clinical issues. Eur Heart J 1987; 8(Suppl B):57-70.  Back to cited text no. 21    
22.Whelton PK, Appel LJ, Espeland MA, et al. Sodium reduction and weight loss in the treatment of hypertension in older persons: a randomized controlled trial of non-pharmacologic interventions in the elderly (TONE). JAMA 1998;279:839­-46.  Back to cited text no. 22  [PUBMED]  [FULLTEXT]
23.Kumanyika SK, Bahnson J, Bottom J, et al. Race & sex influences on the efficacy of non-pharmacologic step-down therapy in hypertensive older adults. Can J Cardiol. 1997;13(Suppl B):369.  Back to cited text no. 23    
24.Cooper R, Rotimi C, Ataman S, et al. The prevalence of hypertension in seven populations of west African origin. Am J Public Health 1997;87:160-8.  Back to cited text no. 24  [PUBMED]  [FULLTEXT]
25.Kannel WB, Garrison RJ, Dannenberg AL. Secular blood pressure trends in normotensive persons: the Framingham study. Am Heart J 1993;125:1154-8.  Back to cited text no. 25  [PUBMED]  
26.Amery A, Birkenhager W, Brixko P, et al. Mortality and morbidity results from the European Working Party on High Blood Pressure in the Elderly Trial. Lancet 1985;l:1349-54.  Back to cited text no. 26    
27.Dahlof B, Lindholm LH, Hansson L, et al. Morbidity and mortality in the Swedish Trial in old patients with Hypertension (STOP-Hypertension). Lancet 1991 ;33 8: 1281-5.  Back to cited text no. 27    
28.Prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension. Final results of the Systolic Hypertension in the Elderly Program (SHEP). SHEP Cooperative Research Group. JAMA 1991;265: 3255-64.  Back to cited text no. 28    

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Correspondence Address:
Gunnar H Anderson
Department of Medicine, Slocum-Dickson Medical Group,1729 Burrstone Road, New Hartford, New York, 13413
USA
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PMID: 18212439

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