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 ::  Abstract
 ::  Introduction
 ::  Material and Methods
 ::  Results
 ::  Discussion
 ::  References
 ::  Article Tables

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ARTICLE
Year : 1977  |  Volume : 23  |  Issue : 3  |  Page : 124-126

Adrenocortical function in renal hypertension


Department of Human Metabolism, Chest Diseases and Pharmacology, L.L.R.M. Medical College, Meerut, India

Correspondence Address:
R K Singh
Department of Human Metabolism, Chest Diseases and Pharmacology, L.L.R.M. Medical College, Meerut
India
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PMID: 614427

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 :: Abstract 

Adrenocortical functions in terms of urinary 17-ketosteroids (17-KS), 17-ketogenic steroids (17-KGS); 17-hydroxycortico­ steroids (17-OHCS) and aldosterone levels have been evaluated in 25 renal hypertensive patients in the present study. Urinary 17-­KS, 17-KGS and 17-OHCS were within normal limits; however, aldosterone was elevated markedly in all the patients of renal hypertension. Thus, it appears that there exist a relation between this salt retaining steroid and renal hypertension.



How to cite this article:
Singh R K, Gupta D K, Singh R C. Adrenocortical function in renal hypertension. J Postgrad Med 1977;23:124-6

How to cite this URL:
Singh R K, Gupta D K, Singh R C. Adrenocortical function in renal hypertension. J Postgrad Med [serial online] 1977 [cited 2014 Oct 30];23:124-6. Available from: http://www.jpgmonline.com/text.asp?1977/23/3/124/42764



 :: Introduction Top


The exact relationship between the adrenocortical steroids and the patho­genesis of hypertension is not clearly known. Although the available experi­mental evidence tends to suggest the im­portance of steroids in the production and maintenance of hypertension [2],[3],[12],[13] their clinical implication is poorly under­stood. Plasma and urinary glucocorti­coids have been reported to be within normal limits in essential benign hyper­tension. [17] On the other hand altered clearance rate of 17-hydroxycorticoids have also been demonstrated in essential hypertension. [8] Similarly the role of aldosterone in metabolic alterations of malignant hypertension is well known. [9],[15] However, little is known about urinary corticosteroids in renal hypertension.

Therefore in the present study an at­tempt was made to evaluate adrenocorti­cal function in terms of urinary 17-keto­steroids (17-KS), 17-ketogenic steroids (17-KGS), 17-hydroxycorticosteroids (17-OHCS) and aldosterone levels in renal hypertensive patients.


 :: Material and Methods Top


Twenty five patients of renal hyper­tension were selected for the evaluation of adrenocortical function in the present study. The ages of these patients range­d between 25 and 65 years. Some of these patients were admitted for treat­ment of some or the other type of nephrourinary diseases like chronic urinary tract infection or pyelonephritis. However, the criteria of diagnosis in these patients were: (1) evidence of hypertension without any cardiovascular or endocrinal disease, (2) clinical evidence of acute or chronic urinary tract infection supplemented with micro­scopic and culture studies of urine, (3) presence of varying degrees of renal in-­absence of any clinical feature sugges­tive of adrenocortical dysfunction. 24­hour urine sample of each patient was col­lected and subjected for the estimation of 17-KS, 17-KGS, 17-OHCS and aldoster­one levels using standard procedures a, described by King and Wootton. [7] Appleby et a1, [1] Peterson et a1 [14] and Neher and Wettstein [11] respectively. In these cases all medications were with­drawn 4 days before investigating the adrenocortical function. Similar studies were simultaneously carried out on 20 normal controls.


 :: Results Top


The results of the estimations of urinary 17-KS, 17-KGS, 17-OHCS and aldosterone levels in 20 controls and 25 hypertensive patients are presented in [Table 1].

Urinary 17-KS and 17-OHCS levels were found to be within the normal limits and the mean values were 7.1 mg/ 24 hours (SE ± 0.58) and 3.9 mg/24 hours (SE ± 0.27) respectively. Fur­ther, we noticed a slight increase in urinary 17-KGS in these patients (mean 15.0 mg/24 hours, SE ± 1.2) though the difference was insignificant (p > 0.05). However, a marked increase (p < 0.001) in urinary aldosterone levels was observ­ed in patients of renal hypertension with an average excretion of 10.6 µg/24 hours (SE - 1.9) [Table 1].


 :: Discussion Top


In the present study renal hyperten­sive patients exhibited no change in urinary 17-KS and 17-OHCS levels. The urinary 17-KGS excretion was slightly increased in these patients though the difference was not significant as compar­ed with the normals. Similar to the pre­sent study unchanged urinary excretion of cortisol and its metabolites in hyper­tension has been reported. [17] In hyperten­sive patients the levels of glucuronide conjugates of 17-OHCS are decreased and conversely the levels of sulfate con­jugates are elevated. [8] However, in the present investigation the conjugation pattern of 17-OHCS has not been studied. Other studies have also demonstrated normal production rate of cortisol in cases of hypertension. [16] Presumably normal production of cortisol in such situations might be responsible for un­changed urinary corticoid levels observ­ed in the present and similar other studies.

Further, we noticed marked increase in urinary aldosterone levels in renal hyper­tensive patients in the present study. Genest et a1 [4] have also reported increas­ed levels of urinary aldosterone in patients of hypertension. Angiotensin ad­ministration increases the aldosterone levels and in hypertensive patients the angiotensin levels are known to be elevat­ed. [6] Thus, the elevated levels of angio­tensin might contribute to some ex­tent in increasing the aldosterone levels in hypertensive patients. The aldo­sterone secretion rate is known to in­crease in hypertension. [5],[9] Likewise an­other mineralocorticoid, i.e., 18-OH-DOC is also secreted more in hypertension. [10] The increased secretion rate observed consistently in the aforesaid studies may also account for elevated levels of urinary aldosterone noticed in the present study. Thus, it appears that the glucocorticoids are not involved in renal hypertension. However, aldosterone levels are largely influenced in such states.

 
 :: References Top

1.Appleby, J. I., Gibson, G., Norymberskl, J. K. and Stubbs, R. D.: Indirect analysis of corticosteroids. I. The deter­mination of 17-hydroxycorticoids. Blo­chem. J. 60: 453-460, 1955.  Back to cited text no. 1    
2.Borst, J. G. G. and Borst-De Geus, A.: Hypertension explained by Starling's theory of circulatory homeostasis. Lancet. 1: 677-682, 1963.  Back to cited text no. 2    
3.Floyer, M. A.: Experimental hyperten­sion. Effect of nephrectomy and adrenalec­tomy upon blood pressure in hypertensive and normotensive rats. Clin. Sci. 10: 405-421, 1951.  Back to cited text no. 3    
4.Genest, J., Koiw, E., Nowaczynski, W. and Le Boeuf, G.: Further studies on urinary aldosterone in human arterial hypertension. Proc. Soc. Exper. Biol. Med. 97: 678, 1958.  Back to cited text no. 4    
5.Genest, J., Boucher, R., Nowaczynskl, W., Koiw, E., de Champlain, J., Biron, P., Chretien, M. and Marc-Aurede, J.: Hypertension. In "Aldosterone" Ed. by Baulien, E. E. and Robel, P., Blackwell Scientific Publication, Oxford, p. 393, 1964.  Back to cited text no. 5    
6.Kahn, J. R., Skeggs, L. R., Jr., Shum­way, N. P. and Weisenbaugh, P. E.:Assay of hypertension from arterial blood of normotensive and hypertensive human beings. J. Exp. Med. 95: 523, 1952.  Back to cited text no. 6    
7.King, E. J. and Wootton, I. D. P.: Urinary steroids. In "Microanalysis in Medical Biochemistry." J. & A. Churchill Ltd., 4th Ed., London, p. 177, 1964.  Back to cited text no. 7    
8.Kornel, L. and Motohashi, K.: Cortico­steroids in human blood. II. Free and conjugated 17-hydroxycorticosteroids in essential hypertension. J. Clin. Endo­crinol. & Metab. 25: 904-911, 1965.  Back to cited text no. 8    
9.Laragh, J. H., Ulick, S., Januszewicz, V., Kelly, W. G. and Lieberman, S.: Electrolyte metabolism and aldosterone secretion in benign and malignent hyper­tension. Ann. Intern. Med. 53: 259-272, 1960.  Back to cited text no. 9    
10.Melby, J. C., Dale, S. L., Grekin, R. J., Gaunt, R. and Wilson, T. E.: 18-hydroxy­11-deoxycorticosterone (18-OH-DOC) secretion in experimental and human hy­pertension. Rec. Prog. Horm. Res., 28: 287, 1972.  Back to cited text no. 10    
11.Neher, R. and Wettstein, A.: Physicoche­mical estimation of aldosterone in urine. J. Clin. Invest., 35: 800-805, 1956.  Back to cited text no. 11    
12.Page, I. H.: The effect of bilateral ad­renalectomy on arterial blood pressure of dogs with experimental hypertension. Amer. J. Physiol., 122: 352-358, 1938.  Back to cited text no. 12    
13.Perera, G. A. and Blood, D. W.: Presser activity of desoxycorticosterone acetate in normotensive and hypertensive subjects. Ann. Intern. Med., 27: 401-404, 1947.  Back to cited text no. 13    
14.Peterson, R. E., Karrer, A. and Guerra, S. L.: Evaluation of Silber-Porter proce­dure for the determination of plasma hy­drocortisone. Analyt. Chem., 29: 144, 1957.  Back to cited text no. 14    
15.Sambhi, M. P., Levitan, B. A., Beek, J. C. and Venning, E. H.: The rate of al­dosterone secretion in hypertensive pa­tients with demonstrable renal artery stenosis. Metabolism, 12: 498-506, 1963.  Back to cited text no. 15    
16.Vermeulen, A. and Straeten, V. D.: Ad­renal cortical function in benign essential hypertension. J. Clin. Endocrinol. and Metahol., 23: 574-578, 1963.  Back to cited text no. 16    
17.Wallace, E. Z., Christy, N. P. and Jailer, J. W.: Clinical application of the simpli­fied porter-silber method for determining plasma 17-hydroxycorticosteroids. J. Clin. Endocrinol. & Metabol, 15: 1073-1088. 1955.  Back to cited text no. 17    



 
 
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