Clinical science and molecular medicine. Supplement最新文献

1. Aorta homogenate contains renin-like activity which on incubation generates angiotensin I over a wide pH range. 2. Rat aortic renin measured at an incubation pH of 6.5 rose and fell in parallel to plasma renin with salt depletion and salt-loading respectively. Renin little relationship with plasma renin. 3. Aortic renin (pH 6.5) was elevated in Goldblatt-two kidney hypertension and slowly fell for 24h after bilateral nephrectomy whereas the fall in plasma renin was complete by the first hour. Aortic renin (pH 5.3) was also high, but did not fall after bilateral nephrectomy. 4. Aortic renin (pH 6.5) is probably derived from plasma renin whereas renin measured at pH 5.3 is probably a tissue renin. 5. The prolonged half-life of aortic renin (pH 6.5) explains the observation that the renin-angiotensin system appears to be active in maintaining blood pressure for several hours after bilateral nephrectomy whereas the decline in plasma renin is rapid and does not continue significantly beyond 1 h.

1. Biosynthesis of PGE2 from [14C]arachidonic acid has been found to be lower and PGF2alpha higher in the renal medulla of spontaneously hypertensive (SH) rats than in normal Wistar (NW) rats. 2. Biosynthesis of prostacyclin (PGF1alpha) from [14C]arachidonic acid was decreased in lungs, aorta and heart of SH rats. 3. Metabolism of [3H]PGF1alpha was decreased in renal cortex and lungs and PGE2 increased in SH rats in comparison with NW rats. Thus the lungs of SH rats let more PGF and less PGE enter the systemic circulation. 4. Emotional stress decreased the metabolism of [3H]PGF1alpha in lungs of SH and NW rats, the effect being less in SH rats.

1. The interaction between prazosin and clonidine was studied in anaesthetized rats, pithed rats and in anaesthetized cats. 2. Prazosin diminished the clonidine-induced hypotensive effect in anaesthetized rats, probably via an antagonism at the level of central alpha-adrenoreceptors. 3. In pithed rats, stimulation of the Nervi accelerantes caused tachycardia, which was diminished considerably by clonidine. The antagonism by clonidine was partly reversed by prazosin, suggesting that prazosin possesses a certain degree of presynaptic activity apart from its predominant effect at the postsynaptic alpha-receptor. Piperoxan was more active than prazosin. 4. The central hypotensive effect of clonidine, injected into the left vertebral artery of cats was significantly reduced by prazosin, administered before clonidine via the same route. Intravenously injected prazosin did not diminish the central hypotensive effect of clonidine. The antagonism is, therefore, caused by a central mechanism. 5. The combined application of clonidine and prazosin in antihypertensive treatment is probably not only irrational but ought to be discouraged in view of the interaction between the drugs, which leads to a reduced antihypertensive potency of clonidine.

1. Chlorothiazide twice a day plus atenolol, metoprolol, pindolol and propranolol in single daily doses administered to patients with essential hypertension achieved effective control of blood pressure. 2. Each beta-adrenoreceptor-blocking drug was associated with small, but significant, increases in plasma triglyceride concentrations and suppression of fasting immuno-reactive glucagon concentrations.

1. A single intravenous administration of rabbit tonin antiserum into one-kidney one-clip hypertensive rats restored blood pressure to normal in seven out of ten animals. There was little change in blood pressure in two-kidney one-clip hypertensive, uninephrectomized or sham-operated rats. 2. Infusion of tonin in control rats did not modify arterial blood pressure. However, in indomethacin salt-treated rats a marked increase in arterial blood pressure was observed under tonin infusion. 3. Plasma tonin activity was significantly increased in human essential and renovascular hypertension. 4. These findings strongly suggest that tonin is important in the maintenance of high blood pressure. However, other factors (possibly prostaglandins and sodium) have to be modified in order to activate the tonin--angiotensin II system.

1. A classical 6 point assay in vitro for measuring aldosterone stimulating activity has been developed. 2. The steroidogenic potency of Ile5-angiotensin II was 62% of that given by Val5-angiotensin II. Ile5-angiotensin III (Des-Asp1-Ile5-angiotensin II) was likewise 50% as active as Val5-angiotensin III (Des-Asp1-Val5-angiotensin II). Similar results were obtained in the pressor and myotropic assays. 3. Ile5-angiotensin III and Val5-angiotensin III had only 7% and 16% respectively of the steroidogenic activity of Val5-angiotensin II. 4. Sar1-Ile5-angiotensin II was 2.3 times as potent as Val5-angiotensin II in aldosterone-stimulating activity. The corresponding activities of Me2-Gly1-angiotensin II, Pro1-angiotensin II and Pro31-angiotensin II were 71%, 15% and 3% of Val5-angiotensin II respectively.

1. In normally hydrated rats prostaglandin F2alpha (PGF2alpha) in doses of 5 microgram/100 g body weight given subcutaneously every 2 h (three times) induced a significant increase in urinary kallikrein activity, and in sodium, potassium and water excretion for 8 h after the first injection. In moderately hyperhydrated rats loaded 2.5% of body wt. with 0.5% NaCl solution, PGF2alpha produced similar changes in kallikrein activity and electrolyte excretion. 2. In normally hydrated rats prostaglandin E2 (PGE2) in the same conditions and doses as in 1 had no effect on kallikrein activity, showing a tendency to decrease potassium and water excretion. 3. PGE2 in doses of 5, 12.5 and 25 microgram/100 g body wt. in overhydrated rats given 2.5% and 0.5% NaCl and 5% of tap water/100 g body wt. 1 h later, significantly increased kallikrein activity in the urine collected for 120 min after the injections. A significant decrease in potassium and water excretion was observed with the highest dose. 4. PGF2alpha, had no effect on kallikrein activity in overhydrated rats, but an increase in sodium and a decrease in potassium excretion was seen at the highest dose. 5. The different actions of PGE2 and PGF2alpha may be part of a regulatory mechanism associated with the kallikrein-kinin system which contributes maintainance of extracellular fluid homeostasis.