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Biomedical subjects

R E McCaa

Publications and source records attributed to R E McCaa.

At least 37 records · Page 2Linked to original sources
PubMed1976

Effect of prolonged angiotensin II infusion on thirst.

To determine the effect of prolonged angiotensin II (A-II) infusion on thirst, daily water intake by drinking was measured in dogs during a 4-day control period, a 4-day period of vehicle infusion without A-II, a 10-day period of A-II infusion, and a 4-day recovery period of vehicle infusion without A-II. During the control period and the periods of vehicle infusion in the absence of A-II, daily water intake by drinking in four dogs averaged 118 +/- 20 ml/day (mean +/- SE). During the 10-day period of A-II infusion at the rate of 13.0 ng/kg per min drinking increased to 269 +/- 49 ml/day (paired t; P less than 0.05). Angiotensin II infusion at the rate of 26.0 ng/kg per min produced a sustained increase in water intake in two dogs during an 8-day period of infusion. These results demonstrate that in dogs, prolonged infusion of angiotensin II stimulates the thirst mechanism and that the effect lasts for more than a few days.

Aldosterone↗
PubMed1976

Effectiveness of the aldosterone-sodium and -potassium feedback control system.

This study was conducted to determine the quantitative importance of the aldosterone feedback mechanism in controlling each one of three major factors that have often been associated with aldosterone, namely, extracellular fluid sodium concentration, extracellular fluid potassium concentration, and extracellular fluid volume. To do this, the ability of the body to control these three factors in the face of marked changes in daily sodium or potassium intake was studied under two conditions: 1) in the normal dog, and 2) in the dog in which the aldosterone feedback mechanism was prevented from functioning by removing the adrenal glands and then providing a continuous fixed level of supportive aldosterone and glucocorticoids during the low and high electrolyte intake periods. Under these conditions, removal of feedback control of aldosterone secretion decreased the effectiveness of plasma potassium control by nearly fivefold (39% vs. 8% change in plasma potassium concentration), fluid volume by sixfold (12% vs. 2% change in sodium space) and had no effect on control of plasma sodium concentration (2% change with and without feedback control of aldosterone secretion.)

Adrenalectomy↗
PubMed1976

The natriuretic and hypotensive effects of potassium.

The chronic effects of potassium loading on sodium balance and related variables were studied in two groups of dogs. The first group was intact except for the presence of indwelling arterial and venous cannulas. On the 1st day, increasing daily potassium intake from a normal level (30 mEq/day) to 200 mEq/day produced a 0.47-mEq increase in plasma potassium with a 56% increase (P greater than 0.01) in sodium excretion in spite of a 58% increase in plasma aldosterone concentration. After 6 days of potassium loading the cumulative negative sodium balance averaged 44 mEq while 22Na space decreased 6.7% (P less than 0.025). In this group arterial pressure did not change measurably. The same experimental protocol was repeated in a second group of dogs that were chronically adrenalectomized and maintained on fixed levels of aldosterone (50 mug/day) and hydrocortisone (1 mg/day). With aldosterone levels held constant the same increase in potassium intake produced a 1st day increase in potassium concentration of 1.20 mEq/liter and 217% (P less than 0.001) increase in sodium excretion. After 5 days of high potassium intake, the cumulative negative sodium balance totaled 84 mEq. Sodium space decreased 7.5% (P less than .005) during the course of the 5-day high potassium intake period. Potassium loading caused a fall in mean arterial pressure in this group; pressure fell from the control level of 110 +/- mm Hg to 87 +/- 4 mm Hg (P less than .001) after 3 days of high intake. By the 5th day of the experiment, pressure stabilized at 96 +/- 3 mm Hg, 13% less than (P less than 0.01) the control level. The results suggest that changes in plasma potassium concentration within physiological limits may have long term effects on sodium balance.

Adrenalectomy↗
PubMed1976

Acute and chronic dose-response relationships for angiotensin, aldosterone, and arterial pressure at varying levels of sodium intake.

We examined the acute and chronic dose-response relationships between intravenously infused angiotensin II (A II) and the resulting changes in arterial pressure and plasma aldosterone concentration at varying levels of sodium intake. Sequential analysis of plasma aldosterone at each A II infusion rate resulted in an acute dose-related increase in plasma aldosterone which was markedly attenuated after the first 24 hours of infusion, the final level being directly related to the dose of A II and inversely related to sodium intake. A II infused at 5,15, and 23 ng/kg per min was associated with an initial increase (2nd to 8th hour) in plasma aldosterone to 2,6, and 9 times control values, respectively, in dogs receiving 40 mEq Na+/day. But, after the 1st day, aldosterone averaged only 1, 1.7, and 3 times control values for the next 2 weeks at the same rates of A II infusion. Dogs receiving 120 mEq Na+/day during A II infusion exhibited only a transient increase in plasma aldosterone during the 1st day. Sustained hypertension developed over a period of a week at all doses of A II at normal and high sodium intake, but did not occur at any dose of A II in sodium-depleted dogs. Increasing sodium intake from 40 to 120 mEq/day resulted in higher levels of hypertension, 125% compared to 140% of ocntrol values for dogs infused with A II, 5.0 ng/kg per min. We conclude that primary angiotensin-induced hypertension need not be associated with increased levels of plasma aldosterone, which appears to remain elevated only with amounts of A II greater than those required to sustain a significant degree of hypertension.

Aldosterone↗
PubMed1975

Role of angiotensin II and potassium in the long-term regulation of aldosterone secretion in intact conscious dogs.

The aldosterone response to long-term infusion of angiotensin II and potassium was studied in intact conscious dogs. Plasma aldosterone concentration (PAC), plasma renin activity (PRA), and plasma cortisol concentration (PCC) were determined by radioimmunoassay. In ten dogs maintained on angiotension II infusion (5 ng/kg min-1) for 14 days, PAC increased from 6.9 plus or minus 2.9 to 18.6 plus or minus 4.7 ng/100 ml plasma (mean plus or minus SE) within ten minutes after beginning the infusion, reached a maximum level of 28.3 plus or minus 6.8 ng/100 ml plasma by one hour, and returned to control levels by six hours. PCC increased from 0.6 plus or minus 0.2 to 3.9 plus or minus 1.0 mu-g/ 100 ml plasma within one hour after angiotensin II infusion and returned to control levels by six hours. During the next 14 days of angiotensin infusion, PAC remained at control levels, PRA was undetectable by radioimmunoassay, and mean arterial blood pressure was elevated 29 plus or minus 4 mm Hg above control levels. In ten dogs maintained on KCL infusion (250 mEg/day) for 15 days, PAC increased from 6.8 plus or minus 2.4 to 13.6 plus or minus 3.4 ng/100 ml plasma within 24 hours, averaged 22.4 plus or minus 4.3 ng/100 ml plasma by 48 hours, and remained elevated for the next 12 days, averaging 21.8 plus or minus 5.6 ng/100 ml plasma. During the next 14 days of KCL infusion, serum Kn increased from 4.1 plus or minus 0.3 to 4.9 plus or minus 0.5 ME1/L, and PRA decreased from 1.25 plus or minus 0.3 to 0.65 plus or minus 0.2 ng/ml/hr. PCC averaged 0.73 plus or minus 0.4 mu-g/100 ml plasma in the control samples and failed to change significantly during KCL infusion. These data indicate that chronic angiotensin II infusion into intact conscious dogs at rates capable of maintaining elevated arterial blood pressure results in a transient increase in aldosterone secretion that lasts only a few hours, while chronic infusion of potassium ions at rates that produce a minor increase in serum Kn results in a sustained increase in aldosterone secretion.

Adrenal Cortex↗