Decapitation increases plasma sodium and potassium in the rat.

Sodium, potassium, and osmolality were measured in plasma obtained from conscious and decapitated rats. The sodium and potassium content of plasma derived from blood taken from decapitated rats via arterial cannulae or free-flowing trunk blood was significantly greater than that in conscious animals or animals killed by an overdose of pentobarbital. Plasma osmolality was not different. Hemoglobin was present in the plasma of decapitated rats, suggesting hemolysis. Hemolysis and subsequent release of intracellular potassium may be the cause of the elevated plasma potassium. The cause of the elevated sodium is unclear. This study points out the importance of considering the method of obtaining blood in determinations of plasma levels of biologic substances.

Arteriolar wall thickening in hypertensive rats unrelated to pressure or sympathoadrenergic influences.

We have previously reported that experimental aortic coarctation in rats is accompanied by non-pressure-related increases in the wall-to-lumen ratio (W/L) of cremaster arterioles. To investigate the role of the sympathoadrenergic system in this arteriolar wall thickening, we partially constricted or sham-constricted the abdominal aorta in adrenal-demedullated, 6-week-old rats that had had guanethidine injections to produce peripheral sympathectomy (S rats, n = 17 coarcted, 16 sham-coarcted) and in sham-demedullated, sham-sympathectomized control rats (SS rats, n = 13 coarcted, 15 sham-coarcted). In both SS and S rats with coarctation, tail and femoral arterial and conscious abdominal aortic pressures were not increased but carotid pressures rose by greater than 30% (p less than 0.01), accompanied by 46-75% increases in cardiac ventricular weight/body weight. In coarcted rats, 4-6 weeks after aortic constriction, compared with sham-coarcted rats, whether S or SS, observation of the cremaster microcirculation revealed increased wall area, wall thickness, and W/L of third- to fifth-order arterioles, both in the resting state and after maximal relaxation with topical nitroprusside. For example, in coarcted S rats wall area after nitroprusside was elevated by 24%, 39%, and 37% in third-, fourth-, and fifth-order arterioles (p less than 0.01). These findings indicate that arteriolar wall thickening in hypertension may occur independently of intra-arterial pressure or sympathoadrenergic influences. Humoral growth factors may be involved.

Increased arteriolar wall-to-lumen ratio in a normotensive vascular bed in coarctation hypertension.

In rats with coarctation hypertension, resting resistance and resistance at maximal vasodilation are elevated in the hindquarters, although blood pressure in this vascular bed remains normal. To assess the nature of these non-pressure-related vascular abnormalities, we observed third- to fifth-order arterioles in the cremaster microcirculation using standard techniques and chloralose-urethan anesthesia in rats with coarctation or sham coarctation of the abdominal aorta. Four weeks after clipping, carotid pressure was significantly elevated in coarcted compared with sham-coarcted rats, but femoral pressure was not. The wall-to-lumen ratio and wall thickness in cremaster arterioles was elevated by 12-33% in coarcted compared with sham-coarcted rats in the resting state. After maximal arteriolar relaxation with topical nitroprusside, differences in wall-to-lumen ratio persisted. We also studied the microcirculation of one-kidney normotensive control and one-kidney, one-clip Goldblatt hypertensive rats. Femoral pressure in Goldblatt hypertensive rats was elevated, but changes in the microcirculation were similar to those observed in coarcted rats. These non-pressure-related changes in vascular structure in hypertension may result from systemic neural or humoral influences and/or growth factors local to vascular wall tissues.

Evidence for a vascular sensitizing factor in plasma of saline-loaded dogs.

This study investigates whether plasma extracts previously demonstrated to have natriuretic and antinatriferic activity have effects on vascular reactivity of rat cremaster arterioles. Plasma from hydropenic and saline-loaded dogs was subjected to Diafiltration, and eluted on a strong cation exchange column (SCX). The effects of intraarterial injections of various column fractions on constrictor responses to repeated injections of 33.3 ng of norepinephrine (NE) were used to indicate changes in vascular responsiveness in third order cremaster arterioles. SCX fraction I (void volume) from saline-loaded dogs (FI-S) caused an increase in constrictor response to NE of 101%. Increased vascular responsiveness peaked at 40 minutes and remained significantly elevated (p less than 0.05) for 130 minutes. Fraction I from plasma of hydropenic dogs (FI-H) and fraction III from plasma of saline-loaded dogs (FIII-S) did not increase vascular responsiveness to NE. FI-S shifted the dose response curves for NE, arginine vasopressin, and angiotensin II parallel and to the left relative to control by a factor of 3.05-, 2.95-, and 5.63-fold, respectively, at the 50% constrictor dose. Systemic injections of FI-S, but not FI-H, caused a 10 mm Hg rise in blood pressure at 50 minutes, and blood pressure was significantly elevated for 30 to 90 minutes after injection (p less than 0.01). These data demonstrate a vascular-sensitizing factor in FI-S. The factor appears in the same chromatographic fraction previously demonstrated to contain natriuretic, antinatriferic, and digoxin-like activity. The correlation of these activities with salt loading suggests they are due to the same substance, which may be the putative natriuretic hormone.