Blood Pressure Response In Rats Research Articles

Hemodynamic effects of metalloporphyrin catalytic antioxidants: structure-activity relationships and species specificity

Superoxide plays a role in blood pressure regulation in certain vascular diseases, however, its involvement in regulating basal blood pressure is uncertain. Vascular superoxide concentrations are limited by extracellular superoxide dismutase (EC-SOD), which is highly expressed in the vasculature of most animal species. Metalloporphyrins are low molecular weight, synthetic, redox-active, catalytic antioxidants that act as SOD mimetics. We evaluated the effects of metalloporphyrins on blood pressure in different animal species. The metalloporphyrin AEOL10113 (5-10 micro /kg iv), but not native or polyethylene glycol-CuZnSOD, caused a dose-dependent reduction in blood pressure in anesthetized rats. AEOL10113 had no effect on blood pressure in mice (wild-type or EC-SOD knockouts), guinea pigs, dogs, or baboons at doses up to 5 mg/kg iv Structure-activity studies indicated that metalloporphyrins with high SOD activity were more effective in lowering rat blood pressure than low-activity analogs. The blood pressure effect of AEOL10113 was not attributable to the release of manganese, nor was it affected by inhibitors of nitric oxide synthase (L-NAME) and guanylate cyclase (ODQ, 8-bromo-cGMP, and methylene blue) or nitric oxide scavengers (HbAo). Chlorpheniramine attenuated the effect, suggesting that the blood pressure response in rats is related to histamine release rather than the protection of nitric oxide.

The role of facilitated diffusion in oxygen transport by cell-free hemoglobins: implications for the design of hemoglobin-based oxygen carriers

We compared rates of oxygen transport in an in vitro capillary system using red blood cells (RBCs) and cell-free hemoglobins. The axial P o 2 drop down the capillary was calculated using finite-element analysis. RBCs, unmodified hemoglobin (HbA 0), cross-linked hemoglobin (αα-Hb) and hemoglobin conjugated to polyethylene-glycol (PEG-Hb) were evaluated. According to their fractional saturation curves, PEG-Hb showed the least desaturation down the capillary, which most closely matched the RBCs; HbA 0 and αα-Hb showed much greater desaturation. A lumped diffusion parameter, K*, was calculated based on the Fick diffusion equation with a term for facilitated diffusion. The overall rates of oxygen transfer are consistent with hemoglobin diffusion rates according to the Stokes–Einstein Law and with previously measured blood pressure responses in rats. This study provides a conceptual framework for the design of a ‘blood substitute’ based on mimicking O 2 transport by RBCs to prevent autoregulatory changes in blood flow and pressure.

Influence of hyperthyroidism on blood pressure responses in rats

Influence of hyperthyroidism on blood pressure responses in rats

Mechanisms of the pressor response to intravenous thyrotropin-releasing hormone in the rat.

1. The purpose of this study was to examine the contribution of the sympatho-adrenomedullary system to the blood pressure response to an intravenous bolus of thyrotropin-releasing hormone (TRH) in conscious medullectomized and sham-operated rats. 2. The peak pressor effect of 0.5 mg TRH was significantly increased in rats having no adrenal medulla (+24.2 +/- 1.6 mmHg, mean +/- s.e.m., P < 0.01) as compared to sham-operated animals (+12.2 +/- 3.0 mmHg). 3. Blockade of alpha-adrenergic receptors with phentolamine abolished the pressor effect of TRH in control rats (+2.1 +/- 1.9 mmHg) but did not attenuate the blood pressure response of medullectomized rats (+21.5 +/- 4.7 mmHg). In contrast, beta-blockade with propranolol blunted the blood pressure responsiveness of rats subjected to adrenal medullectomy (+12.4 +/- 2.6 mmHg) but did not modify the effect of TRH in sham-operated controls (+10.9 +/- 2.9 mmHg). 4. The direct in vitro effect of TRH on isolated mesenteric rat arteries was also evaluated. TRH did not induce contractions of isolated arteries. 5. These results suggest that in rats with intact adrenals, the pressor effect of intravenous TRH is mediated primarily by a stimulation of alpha-adrenergic receptors. Adrenal medullectomy appears to enhance the blood pressure response to intravenous TRH. Activation of cardiac beta-adrenoceptors seems to contribute to the blood pressure increasing effect of intravenous TRH in medullectomized animals.

Influence of Gamma-Aminobutyric Acid on the Changes of Blood Pressure in Rats

This is an attempt to investigate the effect of gamma-aminobutyric acid (GABA), a well-known major inhibitory neurotransmitter in the central nervous system, on the blood pressure response in rats and to elucidate the mechanism of its action. GABA injected into a femoral vein of the rat produced a dose-related fall in blood pressure followed by a secondary pressor response.The depressor response evoked by GABA was clearly blocked by pretreatment with chlorisondamine, diazepam and picrotoxin but was unaffected by atropine, prazosin and debrisoquin. GABA-induced pressor responses were significantly attenuated by pretreatment with prazosin or picrotoxin, while not affected by atropine, diazepam, debrisoquin and chlorisondamine.These experimental data suggest that GABA causes biphasically depressor and pressor responses in rats, and that the hypotensive activity evoked by GABA may be exerted through activation of GABAergic receptors and hypertensive activity due to stimulation of the adrenergic alpha-receptors, which appears to be associated with GABAergic receptors.

P-074 - Measurement of gastric mucosal blood flow responses to vasoactive drugs using cross thermocouple and H2 gas clearance methods in comparison with their blood pressure responses in rats

P-074 - Measurement of gastric mucosal blood flow responses to vasoactive drugs using cross thermocouple and H2 gas clearance methods in comparison with their blood pressure responses in rats

O-152 - Serotonergic regulation of blood pressure response in rats. II. An experiment using DOCA rats

O-152 - Serotonergic regulation of blood pressure response in rats. II. An experiment using DOCA rats

Zinc Deficiency in Rats Reduces the Vasodilation Response to Bradykinin and Prostacyclin

The objective of this study was to determine the effect of zinc deficiency on the blood pressure response of rats to intravenously administered doses of two chemically distinct vasodilators, bradykinin (BK) and prostacyclin (PGI2). Immature albino rats were fed a low zinc (<1 ppm) diet based on soybean protein, a similar control diet (100 ppm) ad libitum or the control diet, pair-fed. After 3 wk, the carotid arteries were catheterized for blood pressure measurement and graded doses of the vasodilators were injected as a bolus into a branch of the femoral vein. In one experiment graded doses (0–8 µg/kg body wt) of Bk and in another graded doses (0–400 ng/kg body wt) of PGI2 were injected. In a third experiment the PGI2 doses ranged from 0 to 1000 ng/kg and, in addition to the 3-wk depletion group, two groups were repleted by feeding the control diet for 1 or 4 d. The low zinc diet induced zinc deficiency as evidenced by low rates of gain and low plasma zinc levels and significantly (P<0.05) decreased the blood pressure response (Emax) to both BK and PGI2. Pair feeding had no significant effect on the response; the Emax values as determined by double-reciprocal plots of the data were unchanged by the quantity of control diet consumed. Short-term repletion did not restore the PGI2 response to control values. The data are interpreted as suggesting that zinc deficiency impairs the function of vasodilator receptors in the rat vasculature.

Anteroventral third ventricle and renin-angiotensin system interaction in the two-kidney, one clip hypertensive rat.

To test the peripheral mechanisms of prevention and reversal of two-kidney, one clip (2K1C) hypertension in the rat by lesion of the anteroventral third ventricle (AV3V) region, we studied blood pressure responses in rats to AV3V lesion produced before (n = 8) or after (n = 8) clipping the left renal artery. Two groups of sham-lesioned, clipped rats (n = 9 each) served as controls. At the end of the experiments, saralasin and captopril were given to evaluate the angiotensin-dependent component of blood pressure. To study the influence of the procedures on plasma renin activity (PRA), two parallel groups of rats (n = 26 and 24, respectively) were submitted to similar surgical protocols. We observed that increases in blood pressure were significantly smaller in the previously lesioned compared to previously sham-lesioned animals (delta BP = 21.5 +/- 3.7 vs. 32.9 +/- 2.5 mm Hg, p less than 0.01); also, AV3V lesion almost completely reversed hypertension (BP from 167.5 +/- 2.9 to 136.0 +/- 4.1 mm Hg, p less than 0.001), which was not observed in the sham-lesioned animals (BP from 172.0 +/- 2.8 to 168 +/- 2.7 mm Hg, NS). Saralasin produced a significantly smaller decrease in BP in the lesioned animals compared to those with sham lesions during both prevention and reversal experiments. Similar results were observed with captopril. Previous AV3V lesion did not significantly affect PRA with clipping of the renal artery, but AV3V destruction after hypertension had been established resulted in significantly lower PRA compared to sham-lesioned animals (4.58 +/- 0.72 vs 8.38 +/- 1.79, respectively, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

P-176 - Blood pressure response in rats raised from parathyroidectomized mothers

P-176 - Blood pressure response in rats raised from parathyroidectomized mothers

Blood pressure response in rats to intracisternal administration of choline.

Blood pressure response in rats to intracisternal administration of choline.

O-40) - Presynaptic α adrenoceptors stimulant action of d-methamphetamine on blood pressure response in rats and on isolated aortic strip response in rabbits

O-40) - Presynaptic α adrenoceptors stimulant action of d-methamphetamine on blood pressure response in rats and on isolated aortic strip response in rabbits

Effects of chronic excess salt ingestion. Genetic influence on the development of salt hypertension in parabiotic rats: evidence for a humoral factor.

Parabiosis has been found to modify the expected blood pressure response of rats from two strains with opposite genetic propensities for experimental hypertension. When a member from one strain was united in parabiosis with a member from the other and both were maintained on high NaCl diet, the rat from the strain ordinarily resistant to it rapidly developed hypertension, in contrast to appropriate controls from this strain. The development of hypertension in this resistant animal preceded that in its mate from the strain highly sensitive to hypertension. In the latter, both the level of hypertension and mortality were significantly less than in its control. It seems likely that the hypertension observed is the resistant parabiont was initiated in its partner from the sensitive strain. This modification in blood pressures was not observed in the absence of a high NaCl diet. Parabiosis between animals from the same strain did not alter their response. Thus, as in earlier experiences (1-4) the interaction of a nongenetic factor (NaCl) with the appropriate genetic substrate appeared to be necessary for the development of hypertension. The findings are interpreted as evidence that a transmittable humoral influence plays an important role in the pathogenesis of rat hypertension. The presence of this agent is genetically determined but, under the conditions of these experiments, it took the added stimulus of dietary NaCl to demonstrate its existence.