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Biomedical subjects

H W Overbeck

Publications and source records attributed to H W Overbeck.

At least 37 records · Page 2Linked to original sources
PubMed1985

Intestinal hemodynamics in dogs with chronic one-kidney, one-wrapped hypertension.

In pentobarbital-anesthetized dogs with chronic one-kidney, one-wrapped perinephritic hypertension, the status of blood flow and resistance differs among vascular beds. There is normal blood flow with elevated resistance in the limb and elevated blood flow with normal resistance in the ileum. In the present study we investigated the mechanism of elevated flow and normal resistance in the ileum by measuring blood flow, pressure, O2 consumption, reactive hyperemia, pressure-flow relationships, resistance at maximal vasodilation, and nonentrapment (shunting) of 9-microns microspheres in vascularly isolated, blood-perfused ilea of 11 24-h fasted dogs with chronic (greater than 4 wk duration) one-kidney perinephritic hypertension [1KH; PA = 163 +/- 8 (SD) mmHg] and 15 fasted normotensive one-kidney, sham-wrapped dogs (1KC; PA = 108 +/- 7 mmHg). In 1KH ileal blood flow was elevated by 35% (P less than 0.001), but ileal vascular resistance was unchanged. Pressure-flow relationships were similar in hypertensive and normotensive ilea, with little evidence for significant autoregulation in either. We also noted no significant differences in ileal O2 consumption, reactive hyperemia, or resistance at maximal vasodilation. However, we found nonentrapment of microspheres to be a positive function of perfusion pressure (P less than 0.02) and to be increased by 40% during ileal perfusion at levels of perfusion pressure within the hypertensive range (150-200 mmHg). Thus the increased ileal blood flow in 1KH may reflect the effects of a poorly autoregulating tissue, as well as "shunt" flow through pressure-activated channels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Arteriolar responses to norepinephrine and ouabain in early 1-kidney, 1-clip hypertension in rats.

We assessed the role of putative circulating ouabainlike factors on in vivo arteriolar function in rats with very early (less than or equal to 7 days, mean 3 days), benign, one-kidney, one-clip (1K1C) hypertension. Thus we measured vascular responses in vasodilated (nitroprusside or adenosine), vascularly isolated, innervated hindlimb vascular beds of chloralose-anesthetized 1K1C rats perfused with their own blood at 1 ml/min. Complete dose-response curves to norepinephrine in 19 1K1C compared with 25 uninephrectomized (1K) normotensive control rats showed unchanged thresholds and 50% effective dosages. Magnitude of ouabain-induced leftward shifts of the dose-response curve in 29 1K1C and 30 1K rats were similar. In 1K1C, compared with 1K, limb resting resistance was elevated by 45% (P less than 0.001), and limb resistance at maximal vasodilation was elevated by 15% (P less than 0.02). These results provide no evidence in this form and stage of hypertension that humoral ouabainlike inhibitors of the sodium-potassium pump evoke physiologically significant inotropic effects in arterioles in vivo. However, the results suggest that significant increases in arteriolar wall-to-lumen ratio occur in the earliest stages (3 days) of hypertension and probably contribute to the elevated resistance.

Animals↗
PubMed1985

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.

Animals↗
PubMed1976

Abnormal ion and water composition of veins and normotensive arteries in coarctation hypertension in rats.

We examined the water, sodium, and potassium composition of the thoracic aorta, abdominal aorta (plus iliac arteries), and veins (vena cava and portal vein) from rats with aortic coarctation. The aortas of 10 rats (group A) were coarcted above the renal arteries to produce hypertension. Control groups consisted of 10 rats sham-coarcted above and 10 rats coarcted below the renal arteries. In group A rats heart weights and carotid artery pressures were elevated over controls (P less than 0.01), whereas there were no significant differences in femoral arterial pressures. In group A rats both the hypertensive thoracic aorta and the normotensive abdominal aorta contained about 20% more water per unit of wet weight, and about 35% and 60% more sodium and potassium, respectively, per unit of dry weight than did the corresponding portions of aorta from control rats (P less than 0.01). In group A rats water (P less than 0.01), sodium (P less than 0.02), and potassium (P less than 0.05) contents of veins also were increased. There were no significant correlations between level of carotid arterial pressure and magnitude of changes in arterial and venous composition, nor were there significant differences between the magnitude of changes in the normotensive and hypertensive portions of the aorta. These results indicate that in rats abnormalities in vascular wall salt and water content are not necessarily a direct effect of the elevated pressure in hypertension.

Animals↗
PubMed1976

Depressed function of a ouabain-sensitive sodium-potassium pump in blood vessels from renal hypertensive dogs.

Vasodilator responses to acute intra-arterial infusions of K+ are attenuated in dogs with chronic one-kidney perinephritic hypertension in rats with chronic two-kidney Goldblatt hypertension, and in men with essential hypertension. There is evidence that K+ evokes vasodilation by stimulating vascular smooth muscle membrane Na+-K+-activated adenosine triphosphatase, thereby increasing activity of the cellular Na+-K+ electrogenic pump. We therefore proposed that there may be an underlying decrease in the operation of this pump in vascular smooth muscle of hypertensives. The operation of the cellular Na+-K+ pump may be estimated by measurement of rubidium uptake. Thus, so further investigate our hypothesis, we measured 86Rb uptake in small mesenteric arteries and splanchnic veins from 12 dogs with chronic uncomplicated one-kidney perinephritic hypertension and from 12 normotensive control dogs. Vessels were excised under thiamylal anesthesia and incubated in cold medium (plasma or Krebs-Henseleit solution) for sodium loading and then the velocity of 86Rb uptake was estimated in the absence of or in the presence of ouabain, a specific inhibitor of the Na+-K+ pump. In neither arteries nor veins was there evidence for differences between hypertensives and normotensives in the ouabain-insensitive uptake of 86Rb. In contrast, the ouabain-sensitive 86Rb uptake was depressed by 42% in arteries (P less than 0.05) and by 49% in veins (P less than 0.01) from hypertensive dogs, if incubated in the dog's own plasma. These results indicate that the activity of a ouabain-sensitive Na+-K+ pump may be depressed in vascular tissue from dogs with chronic one-kidney perinephritic hypertension. Because the Na+-K+ pump in vascular smooth muscle is probably electrogenic, such an abnormality, by partially depolarizing the muscle cell membrane, would help to account for the elevated vascular resistance found in these dogs.

Adenosine Triphosphatases↗
PubMed1976

Bioassay in vivo for circulating vasoactive agents after renal artery constriction in dogs.

We used the gracilis muscle vascular bed to bioassay blood from the two renal veins, vena cava, and aorta continuously for the presence of vasoactive agents before and for 45 minutes after partial occlusion of the left renal artery in dogs. Compared to comparable blood samples from control dogs, left renal venous, vena caval, and aortic blood, but not right renal venous blood, from dogs with renal artery constriction developed vasoconstrictor activity. This was associated with increased renin concentration in plasma from the left renal vein and the vena cava and an increase in systemic arterial pressure. In dogs pretreated with indomethacin, blood from the right renal vein also showed vasoconstrictor activity. Pretreatment with antirenin serum abolished all of the differences between control and experimental dogs. These findings suggest that during acute unilateral renal artery constriction the constricted kidney releases renin and the contralateral kidney releases prostaglandins in sufficient quantity to produce systemic vascular effects.

Animals↗
PubMed1976

Decreased venous compliance in dogs with chronic renal hypertension.

Femoral vein (FV) pressure-volume relationships were measured in vitro in 14 dogs with chronic (more than 4 weeks), one-kidney perinephritic hypertension and in 13 unilaterally nephrectomized normotensive control dogs. Segments of FV were also examined histologically and analyzed for their water and electrolyte contents. Compared to controls: (I) the FV pressure-volume curves of hypertensive dogs were shifted toward the pressure axis (P is less than 0.05); (ii) calcaulated vagous compliance in the pressure range of 0-15 mm Hg was decreased (P is less than 0.05); and (iii) the water and sodium contents of vwins from hypertensive dogs were increased (P is less than 0.05). Histological examination of the FV from hypertensive and control dogs did not reveal significant differences. The findings indicate that the decreases in venous compliance that we have previously observed in the early stages (less than 4 weeks) of perinephritic hypertension in dogs persist into the chronic stage of hypertension. Venous wall "edema" may account for the decreased venous compliance in this form of hypertension.

Animals↗
PubMed1975

Mesenteric hemodynamics in early experimental renal hypertension in dogs.

To investigate mesenteric hemodynamics in early perinephritic hypertension, we measured blood flows and intravascular pressures in innvervated, collateral-free, naturally perfused loops of ileum in 50 male mongrel dogs anesthetized with sodium pentobarbital. In addition, we studied venous pressure-volume relationships in temporarily occluded segments of mesenteric veins in vivo and in excised segments of mesenteric veins in vitro. In 10 dogs (group H-1), one kidney was wrapped in silk 11 days before study; in 15 other dogs (group H-2), one kidney was wrapped 4 weeks before study and the other was removed 2 weeks before study. Twenty-five additional dogs were prepared as normotensive controls: in 10 one kidney was sham-wrapped (group C-1), and in 15 one kidney was sham-wrapped and the other was removed (group C-2). A significant rise in mean arterial blood pressure occurred in groups H-1 and H-2. Compared to controls, (1) ileal blood flow in the hypertensive dogs (H-1 plus H-2) was increased by 17% (P smaller than 0.05), (2) calculated ileal vascular resistances (total and segmental) were unchanged (P smaller than 0.05), and (3) in vivo and in vitro mesenteric vein pressure-volume curves of H-2 (but not of H-1) hypertensive dogs were shifted in the direction of the pressure axis (P smaller than 0.05). These data suggest that in the early stages of perinephritic hypertension in dogs (1) ileal blood flow is increased. (2) ileal vascular resistance is not elevated, and (3) mesenteric venous compliance is reduced. Analysis of the venous pressure-volume curves suggests that the decreased venous compliance is attributable to factors other than smooth muscle contraction.

Animals↗
PubMed1975

Similar vasoconstrictor responses to calcium in normotensive and esssential hypertensive men.

To study limb vascular responses in man to elevations in plasma calcium concentrations, we infused test isosmolar solutions of CaCl2 (0.115, 0.230, and 0.460 meq calcium/min) and NaCl and control isosmolar solutions of NaCl into the brachial arteries of 10 normotensive men and eight men with essential hypertension of mild to moderate severity. Limb blood pressures were monitored, limb blood flow was measured by indicator-dilution, and limb vascular resistance was calculated as mm Hg/ml flow/min/100 cm3 limb volume. Measured concentration of calcium in limb venous plasma during infusion of 0.460 meq calcium/min was 11.5 +/- 0.8 meq/liter (mean +/- SEM) with individual values ranging up to 20 meq/liter. Changes in limb venous serum sodium, potassium, magnesium, and osmolality were similar during control and CaCl2 infusions. Decreases in limb venous blood hematocrit during CaCl2 infusions were the same or greater than those during control infusions. The infusions did not significantly change systemic blood calcium concentration or blood pressures. Limb blood flow decreased and resistance increased in response to CaCl2. Increments averaging as little as 2.2 meq/liter elevated limb resistance by about 45%. Log dose-response curves were linear. Responses did not differ in normotensives and hypertensives (P greater than 0.8). We conclude that the vascular response to acute elevation of plasma calcium concentrations up to 20 meq/liter in the limb oman is an impressive vasoconstriction. We found no evidence for abnormal vascular responses to calcium in essential hypertensive men.

Arteries↗
PubMed1975

Vascular responses to plasma hypoosmolality in man.

To study limb vascular responses to plasma hypoosmolality in man, we infused test solutions of hypoosmolar NaCl (145 mOsm/kg) and control solutions of isosmolar NaCl (290 mOsm/kg) into the brachial arteries of 14 mornotensive and 13 essential hypertensive patients. Limb blood pressures were monitored, limb blood flow was measured by indicator-dilution, and limb vascular resistance was calculated as mmHg/ml flow/min/100 cm3 limb volume. The infusions did not significantly change systemic plasma osmolality, sodium concentration, or blood pressure. Compared to control infusions, the hypoosmolar infusions decreased limb venous plasma osmolality and serum sodium concentrations by an average of 12 mOsm/kg and 7 mEq/1, respectively. Compared to control infusions, limb venous serum concentrations of potassium, calcium, magnesium, or blood hematocrit were not altered by the hypoosmolar infusions. In response to the hypoosmolar infusions, limb resistance increased by 28% in normotensives and by 26% in hypertensives. We conclude that the acute local vascular response to a small reduction in plasma osmolality in the limb of man is a large increase in vascular resistance. We found no evidence for abnormal responses to plasma hypoosmolality in essential hypertensives.

Adult↗
PubMed1975

Vasodilator responses to K+ in genetic hypertensive and in renal hypertensive rats.

Vascular responses to K+ were studied in 37 genetically hypertensive (GH) rats of the New Zealand strain, 12 weight-matched and 11 age-matched normotensive control rats, 21 renal hypertensive (RH) rats with one renal artery clipped and the other kidney untouched, and 18 sham-clipped normotensive control (N) rats, under intravenous chloralose and pentobarbitol anesthesia. KCI in an isosmolar solution, delivering 1.84 X 10(-3), 3.07 X 10(-3), or 4.60 X 10(-3) mEq. K+ per minute was infused intra-arterially into the isolated pump-perfused (blood, 1 ml. per minute) hindlimb vascular beds, increasing measured limb arterial plasma [K+] up to 12 mEq. per liter without changing arterial pressure. The K+ infusions at all three rates reduced limb resistance (P less than 0.01). There was a linear correlation (P less than 0.01) between initial limb resistance and magnitude of response. Analysis of covariance indicated that there were no significant differences between responses in GH and normotensive control rats (P less than 0.1). In contrast, responses in RH rats were decreased (P less than 0.01) when compared to responses in N and GH rats. Thus, the vascular response to K+ is attenuated in renal hypertensive rats, as we have previously found in renal hypertensive dogs and essential hypertensive men, suggesting an underlying defect in vascular K+ metabolism. This abnormality is apparently not shared by genetically hypertensive rats of the New Zealand strain.

Animals↗
PubMed1974

Attenuated vasodilator responses to K+ in essential hypertensive men.

To study limb vascular responses to K(+) in man, paired intrabrachial arterial infusions of isosmolar NaCl (control) and isosmolar KCl (0.077, 0.154, and 0.307 meq K(+)/min) in isosmolar NaCl were made in 20 normotensive men and 20 men with essential hypertension of mild to moderate severity. Limb blood pressures were monitored, limb blood flow was measured by indicator-dilution, and limb vascular resistance was calculated as mm Hg/ml flow/min/100 cm(3) limb volume. Measured concentrations of K(+) in limb venous plasma during infusion of 0.307 meq K(+)/min ranged from 4.8 to 9.0 meq/liter. Changes in limb venous hematocrit, sodium, calcium, magnesium, and osmolality were similar during control and KCl infusions. The infusions did not significantly change systemic blood K(+) concentration or blood pressures. Compared to NaCl, KCl decreased limb resistance (P < 0.05) in both normotensives and hypertensives, in a dose-related manner. Resting limb vascular resistances (IR) in hypertensives were greater (P < 0.05) than those in normotensives. Despite a positive correlation (P < 0.05) between IR and magnitude of response to K(+), responses in hypertensives to K(+) were not greater than those in normotensives. Further, analysis of covariance indicated that responses to 0.307 meq K(+)/min in hypertensives as a group were, in fact, less (P = 0.02) than those in normotensives. These results indicate that the vasodilator response to K(+) may be attenuated in a significant proportion of essential hypertensive men, as it is in renal hypertensive animals. These abnormal responses to K(+) in hypertensives may indicate an underlying defect in vascular K(+) metabolism.

Adult↗