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Biomedical subjects

G S Stokes

Publications and source records attributed to G S Stokes.

At least 109 records · Page 6Linked to original sources
PubMed1974

Renal hypertension in rats immunized against angiotensin I and angiotensin II.

Rats, actively immunized against angiotensin I (AI) and angiotensin II (AII), were subjected to unilateral renal artery constriction to determine whether the resulting hypertension, which may still ensue in the animal immunized against AII, could be prevented by such combined immunity. Sustained immunity to both AI and AII neither changed preoperative blood pressures of the rats from those of control mock-immunized rats nor altered the incidence or severity of renal dip hypertension. Vascular hyperresponsiveness to small quantities of free angiotensin could not be invoked to explain the hypertension, for there was no significant difference between mock-immunized hypertensive animals, and those remaining normotensive, regarding pressor sensitivity to intravenous AI, AII, renin, and norepinephrine. (AI + AII)-immunized hypertensive rats required AI doses averaging 260 times greater than nonimmune hypertensives to elicit equipressor responses, and were refractory to renin, but not to norepinephrine. Thus, while previous studies have not excluded direct participation of endogenous AI in renal clip hypertension in rats, evidence from our experiments makes it extremely difficult to sustain any pressor function therein for circulating AI or AII. Our results also preclude involvement of AII produced from circulating AI by conversion within arteriolar walls, close to receptor sites, since AI immunity would block this mechanism of action.

Angiotensin II↗
PubMed1974

Beta-blockers and plasma renin activity in hypertension.

Long-term treatment with propranolol was shown to produce a sustained suppression of the renin-aldosterone system in hypertensive patients, despite concurrent diuretic treatment. However, the antihypertensive effect of this treatment correlated poorly with its effects on plasma renin activity and urinary aldosterone excretion. When prindolol, another beta-adrenergic blocking drug, was substituted for propranolol, blood pressure control was retained, but there was a prompt rise in plasma renin activity, which was not attributable to changes in electrolyte balance. These observations suggest that the antihypertensive action of propranolol and other beta-blockers does not result from their effects on plasma renin activity.

Adolescent↗
PubMed1974

Comparison of the effects on renin release of beta adrenergic antagonists with differing properties.

Continuous 6-h infusions of the beta adrenergic blockers d,l-propranolol or oxprenolol significantly reduced plasma renin activity (PRA) and mean blood pressure in the resting rabbit and prevented the stimulatory effects of isoproterenol on renin release and heart rate. These actions were due to blockade of beta receptors, for the inactive isomer, d-propranolol, had no effect. Despite sustained high plasma concentrations of d,l-propranolol (0.2 mug/ml) in the unstimulated animal, PRA did not fall below 36% of control values, suggesting that basal renin secretion is maintained partly by factors other than beta adrenergic mechanisms.Prindolol, another beta blocker, also abolished the effects of isoproterenol on renin and on the heart, and reduced blood pressure in the resting animal. However, prindolol increased resting PRA and heart rate, and in animals already receiving d,l-propranolol, it raised PRA and heart rate without further altering blood pressure. This suggests that the effect on PRA of prindolol was due to its intrinsic sympathomimetic activity and not hypotension-mediated mechanisms. The observation that the blood pressure-lowering effect of prindolol was associated with a rise in PRA, while another beta antagonist, H 35/25, lowered PRA but had no effect on blood pressure, indicates that the hypotensive action of beta blockers is unrelated to their effects on renin release. In both unstimulated and isoproterenol-challenged animals, only blockers possessing beta-1 receptor affinity (d,l-propranolol, oxprenolol, prindolol, practolol, and metoprolol) affected heart rate, while effects on PRA were more prominent with agents possessing beta-2 activity (d,l-propranolol, oxprenolol, prindolol, and H 35/25). Thus, the changes in PRA caused by the beta adrenergic blockers appear to be dependent upon the summation of their direct effects, antagonistic or sympathomimetic, on beta-2 adrenergic receptors regulating renin release.

Adrenergic beta-Agonists↗
PubMed1970

Relevance of salt, water, and renin to hypertension in chronic renal failure.

Blood pressure control was examined in 75 patients with end-stage renal failure treated by regular twice-weekly haemodialysis. Dietary sodium was restricted and extracellular fluid was removed by ultrafiltration until blood pressure was normal or signs of salt depletion were observed. Failure of these measures constituted an indication for nephrectomy. Of the 75 patients, 18 were never hypertensive, 46 had hypertension which could be corrected by salt and water depletion, and 11 had persistent hypertension which could not be controlled in this way. Nine of these 11 patients underwent bilateral nephrectomy; in each of the seven in whom the post operative result could be evaluated the blood pressure returned rapidly to normal.Plasma renin activity, measured in 34 subjects, was raised above normal in six out of nine patients whose blood pressure could not be controlled by salt and water depletion and in one of the 11 patients whose blood pressure could be so controlled, but was within the normal range in all nine normotensive patients. The mean level of plasma renin activity in the first group was significantly higher than that of each of the other two groups.There was a significant correlation between hypertension during dialysis and after transplantation, suggesting that, in addition to renin, there is a non-renal factor which predisposes certain patients to hypertension in the presence of salt and water excess.

Chronic Disease↗