The effects of oral calcium loading on the development of hypertension were studied in spontaneously hypertensive rats (SHR). Forty-eight male SHR were divided into four groups according to treatment: control, calcium, deoxycorticosterone (DOC) and DOC + calcium. Both calcium groups received ad libitum 1.5% CaCl2 as drinking fluid. The DOC animals were injected with a mineralocorticoid, deoxycorticosterone trimethyl-acetate, 25 mg/kg, s.c., once a week. Systolic blood pressure (BP) was measured once a week by the tail cuff method. During the nine-week study, the development of hypertension was enhanced in the DOC group, while in the calcium group a blood pressure-lowering effect was observed when compared to the controls. Calcium also abolished the hypertensive effect of DOC. The maximal velocity of calcium transport was higher in "inside-out"-vesicles of red blood cells as compared to controls in both calcium-supplemented groups. DOC treatment resulted in elevated sodium and potassium contents in tail artery tissue, while the effect of the combination of DOC + calcium was equal to controls. On the other hand, the tissue Na:K ratio was decreased in both tail artery wall and heart in the calcium group. Calcium treatment diminished the excretion of phosphate in both groups, while the plasma phosphate concentration was lowered in the calcium group. In mesenteric arterial rings, DOC impaired nitroprusside-induced relaxation, while the relaxation was enhanced compared to control in both the calcium and DOC + calcium groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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Renal denervation delays the development of hypertension in spontaneously hypertensive (SH) rats. The influence of bilateral surgical renal sympathectomy, verified by fluorescence microscopy, on blood pressure and plasma renin activity in SH and normotensive rats (170-180 g before the sympathectomy) was studied. Neither in SH nor in normotensive rats, did the preoperative systolic blood pressure in the renal-sympathectomized group differ from that in the sham-operated controls. After the sympathectomy, blood pressure in the SH rats increased in 4 weeks only insignificantly, from 160 +/- 3 to 172 +/- 6 mmHg, while that in the sham-operated SH rats rose from 163 +/- 5 to 191 +/- 5 mmHg. In normotensive rats, blood pressures in both the renal-sympathectomized and sham-operated groups remained at the pre-operative levels. Thirty days after the operations, plasma renin activity or plasma kininogen in the renal-sympathectomized group did not differ from that in the sham-operated one either in SH or in normotensive rats. The results suggest that the delay in hypertension development produced by renal sympathectomy in SH rats is not mediated by a reduction in renin secretion.

The effects of single oral doses of the angiotensin converting enzyme (ACE) inhibitor quinapril (CI-906) 40 mg and the cardioselective beta-adrenoceptor blocker atenolol 100 mg on sympathetic and parasympathetic function and on exercise capacity have been studied in 8 healthy young men. The trial followed a double-blind, placebo controlled, randomized cross-over design, with at least one week between treatments. Blood pressure (BP) and heart rate (HR) at rest were slightly reduced by atenolol but were not affected by quinapril. Atenolol impaired the sympathetically mediated increases in HR and BP caused by standing, immersion of the hand into melting ice, the Valsalva manoeuvre and isometric forearm exercise. Quinapril did not influence those responses nor the vagally mediated bradycardia of the diving reflex. Atenolol, however, augmented the vagal bradycardia, presumably by sympathetic inhibition. In a dynamic bicycle ergometer test with a stepwise increasing work load, exercise performance was decreased by atenolol but not by quinapril. Inhibition of the renin-angiotensin system by quinapril was shown by a marked decrease in serum ACE activity and a several-fold increase in plasma renin activity (PRA). Atenolol produced a moderate reduction in PRA. Before or during exercise, plasma noradrenaline and adrenaline were not influenced by either drug. The results indicate that, unlike the atenolol-induced beta-adrenoceptor blockade, ACE inhibition by a single dose of quinapril had no clear effect on autonomic nervous function or exercise capacity.

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