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Biomedical subjects

F Gross

Publications and source records attributed to F Gross.

At least 145 records · Page 8Linked to original sources
PubMed1976

Changes in vascular smooth muscle sensitivity to vasoconstrictor agents induced by corticosteroids, adrenalectomy and differing salt intake in rats.

1. Isolated hind limbs of rats were perfused and vascular smooth muscle sensitivity to noradrenaline, methoxamine and potassium chloride was measured and dose-response curves were obtained. 2. The sensitivity of vascular smooth muscle to noradrenaline is attenuated by adrenalectomy and low sodium diet; it is enhanced by corticosterone. High sodium diet or administration of deoxycorticosterone did not alter the dose-response curve significantly. 3. The increased sensitivity of vascular smooth muscle after corticosterone treatment is not related to changes in the contractile protein or alterations in the neuronal uptake and extraneuronal metabolism of noradrenaline. 4. These results suggest that the increased sensitivity in corticosterone-treated rats may be due to the number of receptors, receptor affinity to noradrenaline, or changes in the functional link between receptor and contractile apparatus.

Adrenal Cortex Hormones↗
PubMed1976

Effects of saralasin on renal function of the rat.

In the isolated perfused rat kidney, saralasin inhibits the vasoconstrictor effect of angiotensin II in a dose-dependent manner. At high infusion rates saralasin, by itself, increases renal vascular resistance and supresses renin release. Such an agonistic effect is not observed in the presence of high concentrations of angiotensin II. In acute renal failure induced by glycerol, saralasin has a beneficial effect on urine volume, solute excretion and plasma urea concentration only when it is administered together with an adequate volume of rat serum.

Acute Kidney Injury↗
PubMed1976

Effects of varying sodium intake on blood pressure and renin-angiotensin system in subtotally nephrectomized rats.

In rats in which the renal mass had been reduced by 70 per cent, the effects of varying sodium intake on blood pressure, serum electrolytes, renin-angiotensin system, and some other parameters that were modified simultaneously were studied. Within 4 weeks, a high sodium diet (750 mEa. per kilogram) resulted in marked hypertension, whereas a standard sodium diet (150 mEq. per kilogram) elevated the blood pressure only slightly. A low sodium diet (less than 0.2 mEq. per kilogram) prevented the rise in blood pressure. In the hypertensive group, the hematocrit values were markedly decreased, indicating the expansion of extracellular and intravascular spaces. The compensatory renal hypertrophy was accelerated by the high sodium diet and retarded during restriction. During low sodium intake, the serum concentration of sodium was diminished and that of potassium elevated. During the high sodium diet, the sodium concentration was unchanged, but the potassium concentration was decreased. Subtotal nephrectomy diminished the plasma angiotensin II concentration, and the renin content of the kidney remnant was lower than that of the kidneys from control animals. Sodium restriction stimulated the renin angiotensin system markedly, whereas high sodium intake suppressed it. After subtotal nephrectomy, elevation of blood pressure, renal hypertrophy, and suppression of the renin-angiotensin system are closely related to sodium intake.

Angiotensin II↗
PubMed1975

Relationship between perfusion pressure and renin release in the isolated rat kidney.

Isolated rat kidneys were perfused with either a modified Krebs-Henseleit solution containing a gelatine preparation (Haemaccel, 35 g/1) or with a suspension of washed bovine red blood cells (RBC). Wh en perfusion pressure (PP) was varied repeatedly in the range between 30 and 210 mm Hg autoregulation of renal plama flow (RPF) was almost complete in RBC perfused kidneys. Changes of PP by steps of 20 mm Hg at intervals of 5 min resulted in an incomplete autoregulation of RPF and glomerular filtration rate (GFR). Renin release (RR) was inversely related to PP in the range between 50 and 150 mm Hg, while perfusion at a pressure below or above that range had no further effect on RR. The most marked increase in RR was obtained, when PP was reduced from 90 to 70 mm Hg. After reduction of PP, an increase in RR was measurable within 1 min, and a maximum was reached after 5 min. In kidneys perfused with a cell-free medium at a PP of 45 mm Hg for up to 30 min, RR remained elevated for the entire period of pressure reduction. Injection of microspheres into the renal artery resulted in a prompt decrease of RPF, GFR and urinary sodium excretion, but the values returned towards control levels within 15 min; RR increased only transiently after a short initial fall.

Animals↗