Biomedical subjects

M W Brands

Publications and source records attributed to M W Brands.

60 records · Page 4Linked to original sources

PubMed1989

Aldosterone and renin inhibition by atrial natriuretic factor in potassium-loaded rats.

This study was designed to determine the effects of synthetic rat atrial natriuretic factor (ANF) on plasma renin activity (PRA) and aldosterone secretion in separate groups of normal and potassium-loaded anesthetized rats. Control rats were fed a normal diet of sodium and potassium and had base-line levels of PRA and aldosterone secretion of 25 +/- 3 ng angiotensin I (ANG I).ml-1.h-1 and 0.56 +/- 0.09 ng/min, respectively. Chronic oral potassium loading for 10 days elevated the plasma potassium concentration, stimulated aldosterone secretion to 1.80 +/- 0.18 ng/min (P less than 0.05), and attenuated PRA to 13 +/- 2 ng ANG I.ml-1.h-1 (P less than 0.05). Infusion of ANF at 45 ng.kg-1.min-1 in potassium-loaded rats lowered aldosterone secretion to 1.32 +/- 0.21 ng/min (P less than 0.05) but did not significantly reduce PRA (11 +/- 2 ng ANG I.ml-1.h-1 (P greater than 0.05). A higher ANF infusion dose of 100 ng.kg-1.min-1 produced a further decrement in aldosterone secretion to 1.15 +/- 0.26 ng/min (P less than 0.05) and also reduced PRA to 3 +/- 1 ng ANG I.ml-1.h-1 (P less than 0.05). In the control rats, aldosterone secretion and PRA were decreased significantly during infusion with both low and high ANF doses. Base-line arterial pressures among experimental groups were not different (P greater than 0.05) and did not change during infusion of ANF in any group. These results indicate that ANF can inhibit chronic potassium-stimulated aldosterone secretion in the rat independently of its inhibitory actions on renin release.

Adrenal Glands↗

PubMed1988

Aldosterone and renin inhibition by physiological levels of atrial natriuretic factor.

This study was designed to examine, in the rat, the inhibition of renin release and aldosterone secretion by physiological plasma levels of atrial natriuretic factor (ANF). Intravascular volume expansion over 30 min with donor blood equal to 3% body weight increased plasma ANF concentration from a base line of 216 +/- 28 to 1,590 +/- 240 pg/ml (P less than 0.001) in sodium-replete rats. Basal plasma ANF levels were decreased to 125 +/- 9 pg/ml in animals fed a low-sodium diet, and the infusion of synthetic ANF into separate groups of these rats at doses of 15 or 45 ng.kg-1.min-1 elevated plasma ANF to 346 +/- 38 and 720 +/- 96 pg/ml, respectively (P less than 0.001 for both values). Infusion of ANF at 15 ng.kg-1.min-1 resulted in a significantly lower plasma renin activity [30 +/- 3 vs. 69 +/- 5 ng angiotensin I (ANG I).ml-1.h-1, P less than 0.05], but there was no difference in aldosterone secretion between control and infused groups (7.00 +/- 0.49 vs. 7.29 +/- 0.95 ng/min, P greater than 0.05). However, the higher ANF dose of 45 ng.kg-1.min-1 did reduce aldosterone secretion approximately 40% to 4.18 +/- 0.36 ng/min (P less than 0.001) with no further suppression in plasma renin activity. In sodium-replete rats, infusion of ANF at 45 ng.kg-1.min-1 resulted in lower plasma renin activity compared with the control noninfused group (14 +/- 4 vs. 22 +/- 2 ng ANG I.ml-1.h-1, P less than 0.05), but aldosterone secretion was not different (P greater than 0.05) between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗

PubMed1988

Effects of calcitonin gene-related peptide on renal blood flow in the rat.

The effects of alpha-rat calcitonin gene-related peptide (alpha-rCGRP) on systemic and renal hemodynamics and on renal electrolyte excretion were examined in normal anesthetized rats. In one group of rats (n = 7), infusions of alpha-rCGRP at doses of 10, 50, 100, and 500 ng/kg/min for 15 min each produced dose-related and significant decreases in mean arterial pressure from a control of 130 +/- 3 mm Hg to a maximal depressor response of 91 +/- 2 mm Hg. During the first three doses of alpha-rCGRP, renal blood flow progressively and significantly increased from a control of 5.0 +/- 0.3 ml/min to a peak level of 6.3 +/- 0.3 ml/min achieved during the 100 ng/kg/min infusion. With the highest infusion rate of 500 ng/kg/min, renal blood flow fell below the control level to 4.5 +/- 0.2 ml/min (P less than 0.05). The responses in renal blood flow and mean arterial pressure were associated with reductions in renal vascular resistance. After cessation of alpha-rCGRP infusions, arterial pressure, renal blood flow, and renal vascular resistance gradually returned toward the baseline values. In another group of rats (n = 9), infusion of alpha-rCGRP for 30 min at 100 ng/kg/min produced a significant reduction in urinary sodium excretion from 0.28 +/- 0.06 to 0.14 +/- 0.5 muEq/min (P less than 0.05). Urine flow and urinary potassium excretion also appeared to decrease, but the changes were not significantly different (P greater than 0.05) from their respective baselines. These results demonstrate that alpha-rCGRP is a potent and reversible hypotensive and renal vasodilatory agent in the anesthetized rat. The data also suggest that alpha-rCGRP may have significant effects on the excretory function of the kidney.

Animals↗

PubMed1987

Atrial natriuretic factor in dogs with one-kidney, one-clip Goldblatt hypertension.

The temporal changes in the plasma concentration of immunoreactive atrial natriuretic factor (ANF) were studied in dogs (n = 5) before and after renal artery constriction to produce one-kidney, one-clip renovascular hypertension. Three days after renal artery constriction, circulating ANF increased from 34 +/- 7 to 344 +/- 129 pg/ml (P less than 0.05) in association with a 38-mmHg elevation of mean arterial pressure and increases in plasma renin and aldosterone levels. Plasma renin and aldosterone remained elevated for 9 days after renal artery constriction. Arterial pressure stabilized at this elevated level of 35-40 mmHg above base line for the duration of the 4 wk after renal artery constriction. Right atrial filling pressure did not change significantly (P greater than 0.05) after constriction of the renal artery. This observation suggests that volume expansion with right atrial distention is not the only stimulus for release of ANF in these hypertensive dogs. Plasma ANF remained significantly elevated above base-line levels for 7 days postconstriction even though a twofold decrease from the maximal response of 344 +/- 129 pg/ml on day 3 to 168 +/- 48 pg/ml on day 7 was observed during this same time interval. Plasma ANF continued to decrease toward prehypertensive levels throughout the remainder of the established phase of the hypertension lasting an additional 21 days of observation. The mechanisms for this observed pattern of plasma ANF are unclear but may involve changes in left atrial distention and stretch as a stimulus for hormone secretion with progression of the hypertension.

Aldosterone↗

PubMedDate not supplied

Renal hemodynamic response to intrarenal infusion of calcitonin gene-related peptide in dogs.

The renal hemodynamic and excretory effects of intrarenal infusions of synthetic beta-human calcitonin gene-related peptide (beta-hCGRP) were examined in normal sodium replete dogs (Group 1, n = 6), in sodium replete dogs pretreated with indomethacin (Group 2, n = 6), and in sodium deplete dogs (Group 3, n = 5). In all groups of anesthetized dogs beta-hCGRP was infused at 5 and 10 ng.kg-1.min-1 for 50 min periods each. In the sodium replete group, beta-hCGRP infusions strikingly increased renal blood flow, but this response was markedly attenuated in the other 2 groups. During beta-hCGRP infusions, the clearance of creatinine also increased significantly in the sodium replete and deplete groups, but not in the indomethacin pretreated animals. No consistent changes in urinary sodium excretion or plasma renin activity were observed with beta-hCGRP infusions in any of the 3 groups of dogs. These results indicate that beta-hCGRP is a potent renal vasodilator and can increase renal blood flow and glomerular filtration. The data also suggest that the renal hemodynamic actions of beta-hCGRP are partially mediated by renal prostaglandins, and that the vasodilatory effects of beta-hCGRP may be antagonized by high circulating levels of endogenous angiotensin II in sodium-volume depletion. Finally, beta-hCGRP does not appear to have significant actions on urinary sodium excretion or plasma renin activity under the experimental conditions of the present study.

Animals↗

PubMedDate not supplied

Cardiovascular and renal effects of calcitonin gene-related peptide in hypertensive dogs.

The systemic cardiovascular and renal effects of synthetic beta-human calcitonin gene-related peptide (beta-hCGRP) were examined in conscious normotensive and one-kidney one-clip (1K-1C) hypertensive dogs. beta-hCGRP was infused intravenously at 10 and 50 ng/kg/min for 75-min periods each. Mean arterial pressure did not change significantly (p greater than 0.05) in either group during low dose infusion of beta-hCGRP, but infusion of beta-hCGRP at 50 ng/kg/min produced a fall in mean arterial pressure from 140 +/- 4 to 116 +/- 6 mmHg (p less than 0.05) in the hypertensive dogs (n = 4) and from 100 +/- 4 to 78 +/- 3 mmHg (p less than 0.05) in the normotensive dogs (n = 4). Heart rates increased significantly during infusion of beta-hCGRP in both groups. Also, renal sodium and potassium excretion decreased (p less than 0.05) in the two groups at both the low and high doses of beta-hCGRP. Creatinine clearance was unchanged in normal dogs and decreased (p less than 0.05) in 1K-1C hypertensive dogs at the high rate of beta-hCGRP infusion. The clearance of p-aminohippurate increased approximately 20% (p less than 0.05) in both groups with the low dose infusion of beta-hCGRP but further increases were elicited only in the normotensive dogs in response to the elevation in the beta-hCGRP infusion rate. Plasma renin and aldosterone levels increased (p less than 0.05) above control levels during the maximum hypotensive response to beta-hCGRP infusion in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗