Systemic and regional hemodynamic effects of dietary calcium supplementation in mineralocorticoid hypertension.

This study was undertaken to determine the systemic and regional hemodynamic effects of long-term dietary calcium supplementation in mineralocorticoid (DOC)-salt hypertension. Systemic and regional hemodynamic measurements were determined by the radioactive microsphere technique in conscious and unrestrained rats (kidneys intact) with DOC-salt-induced hypertension that were pair-fed either a normal calcium (0.6% by weight, n = 12) or a calcium-supplemented (high-calcium) diet (2.5% by weight, n = 12). After 7 to 8 weeks, there were no differences in weight, heart rate, or cardiac output between the two groups. In contrast, the high-calcium rats had a significantly lower mean blood pressure (125 +/- 4 mm Hg, mean +/- SEM) than the normal calcium rats (143 +/- 5 mm Hg); this finding appeared to result predominantly from a reduction in total peripheral resistance. The high-calcium rats had a higher renal blood flow (7.8 +/- 0.5% vs. 6.2 +/- 0.4% cardiac output; p less than 0.05) and lower renal (14.3 +/- 1 vs. 19.3 +/- 2 mm Hg/min/ml/g tissue; p less than 0.05) and jejunal vascular resistance than did the normal calcium rats. Two additional identical groups of normal calcium-and high-calcium-DOC-salt rats (n = 12 each) were also studied. In these rats, serum-ionized calcium decreased significantly (p less than 0.05) from baseline in both groups. Urinary sodium increased in both groups but did not differ significantly. In conclusion, dietary calcium supplementation attenuates the rise in peripheral vascular resistance that accompanies DOC-salt hypertension. This attenuated resistance appears to be relatively selective and is noted particularly in the renal vasculature.

Effect of galactose on systemic hemodynamics and blood flow rate in normal and tumor tissues in rats.

The effect of galactose on systemic hemodynamics and blood flow rate of Walker 256 carcinomas and several normal tissues of unanesthetized, unrestrained female Sprague-Dawley rats was measured, using the radioactive microsphere technique, prior to and at 30 and 60 min after galactose administration (6 g/kg body weight, i.v.). Whereas heart rate remained unchanged following injection, cardiac output (CO) and cardiac index decreased by 35% (P less than 0.05). Mean arterial pressure immediately decreased during the injection but then increased reaching a value 10% (P less than 0.05) above the baseline 30 min following injection. Stroke volume (SV) decreased by 30% (P less than 0.05) and total peripheral resistance increased by 65% (P less than 0.05). Redistribution of blood flow, expressed as %CO, among normal tissues was seen to the brain, kidneys, liver, jejunum, and hindlimb muscle and away from the pancreas, stomach, and skin. Changes in %CO to the spleen, colon, forelimb muscle, and peritumor tissue were not significant. Blood flow rate in most normal tissues either decreased or remained constant following injection. An exception was in the liver where blood flow significantly increased. Blood flow significantly decreased in the tumor (approximately 60%) and this reduction in blood flow was larger than the reduction in CO. These results suggest that (a) the effect of galactose on systemic hemodynamics and blood flow rate are similar to those produced by glucose; (b) reduction in blood flow rate in tumors is due to both systemic and local effects; and (c) changes in blood flow to normal tissues should not be disregarded when using galactose in combination with hyperthermia and/or chemotherapy for cancer treatment.