Cardiovascular effects of whole-body heating in spontaneously hypertensive rats

1978 ◽  
Vol 45 (4) ◽  
pp. 521-527 ◽  
Author(s):  
G. Wright ◽  
E. Knecht ◽  
M. Toraason

The cardiovascular response to severe whole-body heating was examined in anesthetized spontaneously hypertensive (SH) (mean BP = 140 Torr) and normotensive (N) rats (mean BP = 96 Torr). Elevation of colonic temperature to 44 degrees C resulted in an initial increase in arterial pressure (mean BP: SH = 199 Torr, N = 124 Torr) with a subsequent severe hypotension. There was little evidence to suggest that this collapse in systemic pressure was related to a direct heat impairment of cardiac function. It was more likely the result of a progressive venodilation which produced venous pooling and decreased venous return. The arterial blood pressure response to exogenous catecholamine challenge decreased at elevated temperatures. This suggests that there was a deterioration of the vasoconstrictor response and indicated a possible effect of heat at the receptor or effector level. There were significant differences between the responses of normotensive and hypertensive rats to whole-body heating suggesting an enhanced cardiovascular sensitivity in hypertensive rats that may partially explain earlier reports of inferior thermoregulation and heat intolerance in these animals.

2015 ◽  
Vol 10 (2) ◽  
pp. 1934578X1501000 ◽  
Author(s):  
Omar Estrada ◽  
Juan M. González-Guzmán ◽  
María M. Salazar-Bookman ◽  
Alfonso Cardozo ◽  
Eva Lucena ◽  
...  

The Aspidosperma genus (Apocynaceae) represents one of the largest sources of indole alkaloids widely associated with cardiovascular effects. Aspidosperma fendleri, a plant found mainly in Venezuela, has a single phytochemical report in which is revealed the presence of alkaloids in its seeds. This study explored the cardiovascular effects of an ethanolic extract of A. fendleri leaves (EEAF) in spontaneously hypertensive rats (SHR) and its potential bioactive compounds. Using bioguided fractionation, fractions and pure compounds were intravenously administered to SHR and their effects on mean arterial blood pressure (MABP) and heart rate (HR) monitored over time. EEAF induced hypotensive and bradycardic effects as shown by significant reductions in mean arterial blood pressure (MABP) and heart rate (HR), respectively. Bioactivity-guided fractionation led to the isolation of a mixture of two known isomeric triterpenoid glycosides identified by spectral evidence as quinovic acid 3- O-β-rhamnopyranoside and quinovic acid 3- O-β-fucopyranoside. This mixture of triterpenoid saponins induced reductions in MABP and HR similar to those induced by propranolol. Together, these findings indicate that the two quinovic acid glycosides are responsible for the hypotensive and bradycardic effects which suggest their potential use in cardiovascular therapy.


1998 ◽  
Vol 18 (3) ◽  
pp. 305-310 ◽  
Author(s):  
Kazunori Toyoda ◽  
Kenichiro Fujii ◽  
Setsuro Ibayashi ◽  
Takanari Kitazono ◽  
Tetsuhiko Nagao ◽  
...  

Cerebral large arteries dilate actively around the lower limits of CBF autoregulation, mediated at least partly by nitric oxide, and maintain CBF during severe hypotension. We tested the hypothesis that this autoregulatory response of large arteries, as well as the response of arterioles, is altered in spontaneously hypertensive rats (SHR) and that the altered response reverts to normal during long-term antihypertensive treatment with cilazapril, an angiotensin-converting enzyme inhibitor. In anesthetized 6- to 7-month-old normotensive Wistar-Kyoto rats (WKY), 4- and 6- to 7-month-old SHR without antihypertensive treatment, and 6- to 7-month-old SHR treated with cilazapril for 10 weeks, local CBF to the brain stem was determined with laser—Doppler flowmetry and diameters of the basilar artery and its branches were measured through a cranial window during stepwise hemorrhagic hypotension. The lower limit of CBF autoregulation shifted upward in untreated SHR to 90 to 105 mm Hg from 30 to 45 mm Hg in WKY, and it reverted to 30 to 45 mm Hg in treated SHR. In response to severe hypotension, the basilar artery dilated by 21 ± 6% (mean ± SD) of the baseline internal diameter in WKY. The vasodilation was impaired in untreated SHR (10 ± 8% in 4-mo-old SHR and 4 ± 5% in 6- to 7-month-old SHR), and was restored to 22 ± 10% by treatment with cilazapril ( P < 0.005). Dilator responses of branch arterioles to hypotension showed similar attenuation and recovery as that of the basilar artery. The data indicate that chronic hypertension impairs the autoregulatory dilation of the basilar artery as well as branch arterioles and that antihypertensive treatment with cilazapril restores the diminished dilation toward normal.


1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.


1994 ◽  
Vol 71 (4) ◽  
pp. 583-603 ◽  
Author(s):  
Yvonne V. Yuan ◽  
David D. Kitts

The effects of dietary protein on Ca bioavailability and utilization in bone were examined in male spontaneously hypertensive rats (SHR) fed on diets containing either casein (200 g/kg (control), 60 g/kg or heat-damaged (HD) 200 g/kg) or soya-bean protein isolate (200 g/kg (control), 60 g/kg, or HD 200 g/kg). Casein was heat-damaged to limit caseinophosphopeptide (CPP) production in order to evaluate casein enhancement of Ca bioavailability. All diets contained an adequate level of Ca (5 g/kg). A 24 h mineral balance study was performed when animals were 10 weeks old, followed by measurement of in situ paracellular Ca disappearance, femur mineralization and biomechanics at 14 weeks of age. Digestibility of soya-bean and both HD proteins estimated in vitro was reduced compared with native casein. Animals fed on HD and 60 g/kg protein diets exhibited decreased (P < 0.05) body weight gain, dry matter intake and feed efficiency compared with controls. The ileal disappearance of 45Ca was lower (P < 0.05) in animals fed on HD casein and all the soya-bean protein diets. Ca balance was not strongly affected by dietary treatments. A significant (P < 0.05) interaction between protein source and reduced protein intake was observed for femur calcification and physical measurements. Femur bending failure energy and biomechanical force measurements were reduced (P < 0.05) in HD and 60 g/kg casein and soya-bean protein fed animals. These findings suggest that whole-body Ca homeostatic mechanisms were involved in compensating for reduced Ca bioavailability and retention from casein diets modified to reduce protein digestibility and CPP production.


2019 ◽  
Vol 10 ◽  
Author(s):  
Thayane Rebeca Alves-Santos ◽  
Odair Alves Silva ◽  
Hicla Stefany Moreira ◽  
Rosivaldo Santos Borges ◽  
Gloria Pinto Duarte ◽  
...  

1994 ◽  
Vol 266 (4) ◽  
pp. R1148-R1153 ◽  
Author(s):  
A. Bataillard ◽  
J. Sassard

Cardiovascular effects of human recombinant interleukin-1 beta (hrIL-1 beta) were investigated in normotensive rats using a computerized analysis of arterial blood pressure in conscious, unrestrained animals. Intravenous injection of hrIL-1 beta induced a rapid and short-lasting rise in blood pressure associated with a first slight tachycardia followed by a second sustained and pronounced increase in heart rate. These effects occurred in a dose-related manner. Pretreatment with a converting-enzyme inhibitor (perindopril) did not modify the hrIL-1 beta-induced increase in blood pressure. Blockade of beta 1-adrenoceptors (atenolol) prevented the tachycardia, but did not significantly affect the pressor response to hrIL-1 beta. On the contrary, the hrIL-1 beta-induced increase in blood pressure was inhibited by an alpha 1-adrenoceptor antagonist (prazosin), whereas the tachycardia was untouched. Finally, pretreatment with a cyclooxygenase inhibitor (indomethacin) completely abolished the cardiovascular response to hrIL-1 beta. These results suggest that the hrIL-1 beta-induced pressor response and associated tachycardia require the synthesis of prostaglandins and involve a sympathetic nervous system activation but do not depend on the renin-angiotensin system.


1993 ◽  
Vol 265 (5) ◽  
pp. R1184-R1190
Author(s):  
T. Hamakubo ◽  
M. Yoshida ◽  
K. Nakajima ◽  
T. X. Watanabe ◽  
R. Mosqueda-Garcia ◽  
...  

Joining peptide (JP) is one of the major products of proopiomelanocortin (POMC). The biological function of this peptide has not been clarified despite its relative abundance in the pituitary and the hypothalamus. Recently we demonstrated that JP, which was isolated from bovine posterior pituitary, possesses Na pump inhibitor activity. The purpose of this study is to explore the physiological relevance of JP in cardiovascular regulation. For these investigations, we used the synthetic peptides bovine JP (bJP) and COOH-terminally amidated rat JP (rJP), since JP is known to have sequence variability among species. Intracisternal administration of both bJP and rJP in urethan-anesthetized rats evoked similar hypertensive and tachycardia effects. The effects of both peptides were markedly greater in the spontaneously hypertensive rats (SHR) compared with the normotensive Wistar Kyoto rats (WKY). Intravenous bolus injections of rJP at the same doses were without effect. Autoradiography, using 125I-labeled [0Tyr]-rJP as a ligand, revealed specific binding sites for rJP in the dorsal medulla in areas corresponding to the nucleus tractus solitarii (NTS) (extending from approximately 0.4 mm caudal to 1.8 mm rostral to the obex). Microinjections of rJP into the caudal part of the NTS of anesthetized SHR produced dose-related pressor and tachycardic responses. The pressor and tachycardic responses were also observed at the rostral part of the NTS, whereas the injections into the intermediate part of the NTS evoked depressor and bradycardic responses in SHR. These results suggest that at doses tested, the site of JP action resides in the central nervous system, and that JP is a potent neuropeptide in medullary sites known to be pivotal in central cardiovascular regulation. The effect of JP is especially prominent in the genetically hypertensive rat.


2005 ◽  
Vol 288 (2) ◽  
pp. H805-H812 ◽  
Author(s):  
F. A. DeLano ◽  
R. Balete ◽  
G. W. Schmid-Schönbein

One mechanism for organ damage in individuals with arterial hypertension may be due to oxygen free radical production. This study was designed to localize free radicals in a microvascular network of mature spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats. Because glucocorticoids play a role in pressure elevation of SHRs, we investigated their role in microvascular free radical formation. Oxygen radical production in mesentery was detected by tetranitroblue tetrazolium reduction to formazan aided by digital light-absorption measurements. Formazan deposits were observed in the endothelial cells and lumens of all microvessels and in lymphatic endothelia but were fewer in tissue parenchyma. The formazan distribution in younger (14–16 wk old) WKY rats and SHRs was heterogeneous with low values in capillaries and small arterioles/venules (<30 μm) but enhanced deposits in larger venules. Adrenalectomy served to reduce the formazan density in SHRs to the level of WKY rats, whereas dexamethasone supplementation of the adrenalectomized rats caused elevation in the larger venules of SHRs. In older (40 wk old) SHRs, formazan levels were elevated in all hierarchies of microvessels. After pressure reduction was employed with chronic hydralazine treatment, the formazan deposits were reduced in all locations of the microcirculation in both WKY rats and SHRs. Elevated formazan deposits were also found in lymphatic endothelium. These results suggest that oxygen free radical production is elevated in both high- and low-pressure regions of SHR microcirculation via a process that is controlled by glucocorticoids. Older SHRs have higher formazan levels than younger SHRs in all microvessels. Chronic hydralazine treatment, which serves to reduce arterial blood pressure, attenuates tetranitroblue tetrazolium reduction in WKY rats and SHRs even in venules of the microcirculation, which has no micropressure elevation. Free radical production may be a more global condition in SHRs and may not be limited to arteries and arterioles.


Sign in / Sign up

Export Citation Format

Share Document