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Biomedical subjects

H W Overbeck

Publications and source records attributed to H W Overbeck.

58 records · Page 4Linked to original sources
PubMedDate not supplied

Effect of ouabain on arteriolar responses to norepinephrine in chronic, benign, volume-expanded hypertension.

We have reported increases in ouabain-sensitive Rb+ uptake by freshly excised conduit arteries from volume-expanded Dahl salt-sensitive (S) rats and also from rats with chronic (4 to 6 weeks), benign (serum creatinine less than 1.4 mg%) one-kidney, one clip ( 1K1C ) hypertension on high NaCl intake. To assess in vivo arteriolar function in this latter model, and a role for putative circulating ouabain-like factors, we perfused the maximally vasodilated (nitroprusside, 0.015 mg/ml limb blood), vascularly isolated, innervated hindlimb vascular beds of chloralose-anesthetized, water- or saline-drinking 1K1C hypertensive rats with their own blood at 1 ml/min, and measured limb responses to i.a. norepinephrine 0.004 to 128 micrograms, before and during local infusion of ouabain (achieving 2.5 X 10(-5) M in limb blood). Complete dose-response curves in eight 1K1C hypertensive rats were steeper and higher than those in five uninephrectomized (1K) normotensive control rats. However, threshold and ED50 were unchanged. Thus, alterations in the curve in the hypertensive rats represented only structural vascular changes. Ouabain evoked a leftward shift of the dose-response curve in an additional 18 1K1C hypertensive rats and 13 1K normotensive controls. In the hypertensive rats as compared to the controls, there were trends for increases, rather than decreases, in the ouabain-induced shift of the curve. Shifts in 14 rats with chronic 2K1C hypertension did not differ from those in the 1K1C hypertensive rats. Together, these studies in chronic, presumably volume-expanded, low-renin hypertension unaccompanied by renal insufficiency provide no evidence for physiologically significant inotropic effects of circulating ouabain-like pump inhibitor.

Animals↗
PubMedDate not supplied

Attenuated arteriolar dilator responses to calcium in genetically hypertensive rats.

Vascular responses to calcium were studied in 14 genetically hypertensive (GH) rats of the New Zealand strain and 16 weight- and age-matched normotensive parent strain control rats under chloralose-pentobarbital anesthesia. Calcium (chloride or gluconate) in an isosmolar solution was infused intraarterially into the hindlimb vascular bed which was vascularly isolated, innervated, and pump-perfused (blood, 1 ml/min). Increases in limb plasma calcium concentrations up to 30 mEq/liter decreased limb vascular resistance, with no evidence for vasoconstriction. In GH rats decreases in limb vascular resistance in response to increments in limb plasma calcium concentrations of 3.6 to 10.8 mEq/liter were significantly (p less than 0.02) attenuated compared to age-matched controls. When responses in GH were compared to weight-matched controls, similar trends toward attenuation reached significance (p less than 0.02) at Ca2+ increments of 10.8 mEq/liter. In eight other GH rats, we measured total serum calcium concentrations and found them reduced (4.94 +/- 0.08 mEq/liter), especially as compared to values in eight rats of an unrelated Wistar strain (5.42 +/- 0.04 mEq/liter; p less than 0.05). These experiments provide evidence that, over physiological ranges, calcium relaxes arteriolar smooth muscle in rats and that this vasodilation is attenuated in genetically hypertensive rats. Thus, both the lower serum levels of calcium and the attenuated responses to calcium may contribute to the elevated peripheral vascular resistance and hypertension in these rats.

Analysis of Variance↗
PubMedDate not supplied

Relationship of vascular sodium-potassium pump activity to intracellular sodium in hypertensive rats.

The activity of the sodium-potassium (Na+-K+) pump in arterial tissue from rats with chronic DOCA-salt or one-kidney Grollman renal hypertension was assayed in vitro as the rate of ouabain-sensitive 86Rb+ uptake. Estimates of total cell Na+ and tissue K+ were made by a lithium-substitution method on the same segment of arterial tissue. In both freshly excised tail arteries and aortas, and in aortas after overnight cold storage at 4 degrees C and a 3-hour equilibration at 37 degrees in Krebs-Henseleit, cell Na+ content did not differ significantly between control and hypertensive groups. However, ouabain-sensitive 86Rb+ uptake was increased in arteries from DOCA-salt and renal hypertensive rats as compared to controls. In overnight-stored and 3-hour equilibrated aortic tissue, we then used low Na+ medium to reduce, or monensin, a Na+ ionophore, to increase total cell Na+, to study the relationship between cell Na+ and Na+-K+ pump activity. We observed a sigmoid relationship between total cell Na+ and ouabain-sensitive 86Rb+ uptake in tissue from all groups of rats. However, in tissue from DOCA-salt and renal hypertensive rats, the relationship between cell Na+ and pump activity was shifted, indicating a greater pump activity for each level of total cell Na+ and greater maximal pumping. These data suggest that increases observed in pump activity in in vitro arterial tissue from hypertensive rats may not be solely attributable to elevated cell Na+ content and may also involve increases in number of active sarcolemmal pump molecules per unit tissue weight or in their turnover rate.

Animals↗