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Hypertension. 1989 Apr;13(4):371-7.
Prolonged converting enzyme inhibition in non-modulating hypertension.

Dluhy RG, Smith K, Taylor T, Hollenberg NK, Williams GH.

Endocrine-Hypertension Unit, Brigham and Women's Hospital, Boston, Massachusetts 02115.

Patients with normal- or high-renin non-modulating essential hypertension fail to shift their adrenal sensitivity on a low sodium diet in response to an infusion of angiotensin II (Ang II). In a prior study, 72 hours of converting enzyme inhibition (CEI) partially corrected this subnormal aldosterone response to Ang II in patients with non-modulating hypertension. Since it was uncertain whether the failure to restore normal adrenal responsiveness reflected a continued abnormality or an insufficient duration of CEI, the present study was performed wherein subjects were studied before CEI and then 72 hours and 6 weeks after CEI. Adrenal and renovascular responses were assessed in 13 subjects with normal- or high-renin hypertension in response to an infusion of Ang II (0.3, 1.0, and 3.0 ng/kg/min) in balance on a 10 meq Na+/100 meq K+ diet. Eight of 13 had a normal plasma aldosterone increment above control levels (greater than or equal to 15 ng/dl) and were classified as modulators; the remaining subjects (five of 13) were classified as non-modulators. Enalapril was then administered for 72 hours and 6 weeks, and the assessment of the Ang II dose-response relations was repeated. In the modulators, there was no change compared with levels before CEI in the aldosterone dose-response curve or threshold sensitivity to infused Ang II at either 3 days or 6 weeks after CEI administration. In the non-modulators, CEI for 72 hours partially restored aldosterone responsiveness, but more prolonged CEI for 6 weeks completely corrected the defect, restoring aldosterone responsiveness on a sodium-restricted diet to that seen in modulators and in normotensive control subjects.(ABSTRACT TRUNCATED AT 400 WORDS)

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2538393&dopt=Abstract




Minerva Cardioangiol. 1989 Mar;37(3):111-8.
[Calcium antagonists vs ACE inhibitors in the treatment of essential arterial hypertension in the aged]

[Article in Italian]

Cellamare G, Poppa E, Sgobba G, Bianco G.

Numerous epidemiological studies have shown that systolic and systodisystolic hypertension constitute major risk factors for damaging or fatal cardiovascular accidents in the elderly as well as the young. Furthermore reducing the blood pressure also reduces the risk. In 1983 Fleckenstein investigated the Ca++ and MG++ contact of human arteries and clearly demonstrated that titres of both but especially Ca++ in the arterial wall increased progressively with age. The Authors themselves caused calcinosis of the arterial wall in rats treated with Vitamin D3 and Dihydrotachysterol and were able to prevent the occurrence with Verapamil. It is against this background that the present study compared the efficacy and tolerability of two anti-hypertensive drug groups in the calcium antagonists and the ACE inhibitors (Enalapril Maleate) used individually on two groups of elderly hypertensives. A group of 123 out patients with a mean age of 73 and all suffering from slight-to-moderate hypertension were monitored for 6 months being subjected to the following examinations: clinical assessment including blood pressure measurements lying and standing, biohumoral tests, remote heart X-rays, echocardiography (to establish the Reichek systolic wall stress index) and ECG. The clinical examination and ECG were repeated every 2 weeks for the first 6 months and once a month thereafter. The heart X-rays, echocardiogram and biohumeral tests were performed every 6 months. The patients were divided into two groups I and II and assigned to the selected treatment. The Group I patients were then divided into 3 subgroups and treated with 3 different calcium antagonists (Nifedipine R; Verapamil R and Diltiazem). All group II patients were treated with Enalapril Maleate.(ABSTRACT TRUNCATED AT 250 WORDS)

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2546102&dopt=Abstract




Kidney Int. 1997 Jan;51(1):36-43.
Inhibition of angiotensin-converting enzyme modulates structural and functional adaptation to loop diuretic-induced diuresis.

Beck FX, Ohno A, Muller E, Seppi T, Pfaller W.

Department of Physiology, University of Munich, Germany.

The roles of elevated cell sodium concentrations and the angiotensin-aldosterone system (AAS) in the structural and functional adaptation of the distal tubule and collecting duct system to a chronic increase of sodium delivery were examined using electron microprobe and quantitative morphologic/stereologic analyses. Studies were performed on rats given the loop diuretic torasemide acutely (20 min) or chronically (12 days), either alone or in combination with the angiotensin-converting enzyme (ACE) inhibitor, enalapril. In the sodium-absorbing cells of the distal tubule and cortical collecting duct-that is, in distal convoluted tubule (DCT), connecting tubule (CNT) and principal cells-an acute increase in sodium delivery caused a significant rise in intracellular sodium concentration and rubidium uptake, the latter an index of in vivo Na,K(Rb)-ATPase activity. The elevated cell sodium concentrations returned to, or close to, control values during chronic torasemide treatment. Intracellular rubidium concentrations, measured after a 30-second rubidium exposure, were not different from controls in DCT and CNT cells but were still higher in principal cells. Since, however, the distribution space for rubidium was significantly increased in chronic torasemide animals, rubidium uptake, and hence Na,K-ATPase activity, must have increased in proportion to cell volume in DCT and CNT cells, but more than proportionately in principal cells. When ACE was inhibited during chronic torasemide, the epithelial volume of DCT and cortical collecting duct (CCD) was increased mainly by lengthening and not, as was the case in rats given torasemide alone, by thickening of the tubule wall. Adaptation of the proximal tubule exclusively by lengthening was not affected by inhibition of the ACE. These data indicate that changes in cell ion composition may participate in initiating cell processes leading to adaptation of distal nephron segments to chronically increased salt delivery. Inhibition of the ACE reverses the torasemide-induced increase in apparent Na pump density in principal cells and seems to shift the relationship between hypertrophy and hyperplasia noted in DCT and CCD after chronic torasemide in favor of hyperplasia.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8995715&dopt=Abstract












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