This study was performed with Dahi salt-sensitive (DS) and Dahi salt-resistant (DR) rats to detect differences hi cardiovascular hemodynamics and renal responses that might be involved hi initiating salt-induced hypertension hi DS rats. The effects of 4 weeks of 8% NaCl diet were studied hi conscious, male DR and DS rats hi which vascular and urinary catheters had been previously implanted. Results were compared with those obtained from control groups of DR and DS rats on 4 weeks of 1% NaCl diet. DR rats on 8% salt diet did not develop hypertension, and cardiac output and blood volume were unchanged; glomerular filtration rate, urinary flow, sodium excretion, and plasma atrial natriuretic factor (ANT) increased. DS rats on 8% salt diet developed hypertension, and cardiac output and blood volume increased; glomerular filtration rate, urinary flow, and sodium excretion did not change, despite an increase hi ANF. DS and DR rats on 1% NaCl diet were subjected to ANF infusion. After ANF infusion DR rats had a decreased blood volume and an increased glomerular filtration rate, urinary flow, and sodium excretion; DS rats showed no significant changes hi blood volume, glomerular filtration rate, urinary flow, or sodium excretion. ANF caused vasodilation hi all regions studied hi DR rats; DS rats showed vasodilation hi all regions except the kidney. After acute volume expansion, although both DR and DS rats responded by an increase hi cardiac output, only DS rats developed prolonged hypertension. This finding suggests an inadequate vasodilatory mechanism in DS rats. In response to acute volume expansion, renal resistance decreased hi DR rats but not hi DS rats. It is concluded that the primary hemodynamic disturbance hi DS rats with salt-Induced hypertension is an increase hi cardiac output caused by blood volume expansion hi the absence of any vasodilation. Comparison of the responses of DS and DR rats to high salt diets, ANF infusion, and acute volume expansion indicates that the salt-induced hypertension in DS rats is initiated by a diminished renal response to ANF. (Hypertension 1989;13:612-621) T his study was performed with Dahi saltsensitive (DS) and Dahi salt-resistant (DR) rats to detect differences in cardiovascular hemodynamics and renal responses that might be involved in initiating salt-induced hypertension in DS rats. On the basis of experimental evidence as

In 10 pentobarbitalized dogs, plasma viscosity (Ep) was raised fourfold while apparent blood viscosity (Ea) increased about twofold by two steps of exchange transfusion of 200 ml of plasma with plasma containing high molecular weight dextran (mol wt 500,000, 20% wt/vol). Elevation of Ea was primarily caused by an increase of Ep but not red cell aggregation. As Ea increased, regional blood flow (by 15-microns microspheres) remained constant in most organs but reduced in the small intestine, spleen, and thyroid gland. Vascular hindrance (Z), which reflects the state of vascular geometry, was calculated as flow resistance per Ea. Among various organs, a reduction in Z was noted in the heart, liver, pancreas, kidney, brain, and adrenal gland. In myocardium, there was a progressive reduction of the endocardial-to-epicardial flow ratio, indicating a less profound vasodilation in endocardium than epicardium. These results indicate that dextran-induced hyperviscosity leads to a compensatory vasodilation in several vital organs thus serving to maintain blood flow and nutrient transport.

The effects of alterations in apparent blood viscosity on renal hemodynamics and plasma renin activity (PRA) were studied in dogs anesthetized with sodium pentobarbital. Blood viscosity was altered isovolemically either by changes in hematocrit (Hct) or by an increase in plasma viscosity (dextran administration). Arterial blood pressure and renal blood flow (RBF) remained relatively constant when apparent blood viscosity was elevated by changes in Hct or plasma viscosity. Thus the hyperviscosity of blood was associated with a decrease of renal vascular hindrance, resulting in an essentially unchanged renal flow resistance. The decrease in renal vascular hindrance may result from renal vasodilation. In hyperviscosity induced with dextran, the increase in PRA correlates linearly with the decrease in renal vascular hindrance, with a coefficient of correlation of 0.968 (P less than 0.005). The increase in PRA that resulted when Hct was raised from 25 to 55% also can be correlated linearly with the decrease in renal vascular hindrance, with a coefficient of correlation of 0.953 (P less than 0.005). These results suggest that the decrease in renal vascular hindrance in response to a rise in apparent blood viscosity leads to an increase in PRA.

No abstract

The transvascular leakage of albumin in various organs and tissues was studied with a double isotope technique in rats anesthetized with sodium pentobarbital, given intraperitoneally or intravenously, and in unanesthetized (conscious) rats. 125I-labeled albumin and 131I-labeled albumin were injected into the tail vein 1 hr apart. The albumin permeability index in tissues and organs is indicated by the local ratio (Xa/Ya)/(Xb/Yb), where (Xa/Ya) is the ratio of 125I/131I-albumin activities per g of tissue and (Xb/Yb) is the ratio of 125I/131I-albumin activities per g of blood. If there is no passage of albumin across the capillary membrane over the 1-hr period of study, the permeability index will be equal to one. In unanesthetized rats, the liver, lung, kidney, femoral muscle, and femoral skin were regions with a high albumin permeability index (above 2). In these organs, intraperitoneal and intravenous anesthesia caused a decrease or no significant change of the albumin permeability index. There was no significant albumin leakage over 1-hr period (index not significantly different from 1) in the mesentery, abdominal muscle, abdominal skin, cremaster, heart, and brain of unanesthetized rats. Intraperitoneal anesthesia caused the albumin permeability index to increase to approximately 4 in the mesentery, abdominal muscle, and the abdominal skin, but not in the cremaster, heart, or brain. These results demonstrate that pentobarbital anesthesia when given into the peritoneal cavity causes a significant increase in albumin leakage in the abdominal region.