Acute exercise and gender alter cardiac autonomic tonus differently in hypertensive and normotensive rats

1998 ◽  
Vol 274 (2) ◽  
pp. R510-R516 ◽  
Author(s):  
Margaret P. Chandler ◽  
Stephen E. Dicarlo
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Acute Exercise ◽  
Female Rats ◽  
Male Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Cardiac Autonomic Regulation ◽  
Before And After ◽  
Wistar Kyoto ◽  
And Gender

Arterial pressure (AP), heart rate (HR), cardiac sympathetic tonus (ST), and parasympathetic tonus (PT) were determined in spontaneously hypertensive rats (SHR, 8 male and 8 female) and Wistar-Kyoto normotensive rats (WKY, 8 male and 12 female) before and after acute exercise. Before exercise, hypertensive rats (regardless of gender) had an increased ST (+15 beats/min), increased resting HR (+12 beats/min), and decreased PT (−11 beats/min). Similarly, female rats (regardless of strain) also had an increased ST (+15 beats/min), increased resting HR (+39 beats/min), and decreased PT (−14 beats/min). Hypertensive rats had a significant reduction in AP (−17 ± 3 mmHg), ST (−26 beats/min), PT (−7 beats/min), and HR (−14 beats/min) after exercise. In contrast, AP was not reduced in normotensive rats and ST (+18 beats/min) and HR (+42 beats/min) were increased in female normotensive rats after exercise. However, male normotensive rats had a postexercise reduction in ST (−14 beats/min) and HR (−19 beats/min). In summary, AP, ST, and resting HR were higher whereas PT was lower in hypertensive vs. normotensive rats. Furthermore, females had a higher resting HR, intrinsic HR, and ST and lower PT than male rats. These data demonstrate that gender and the resting level of AP influence cardiac autonomic regulation.

scholarly journals STIM1/Orai1 contributes to sex differences in vascular responses to calcium in spontaneously hypertensive rats

2011 ◽  
Vol 122 (5) ◽  
pp. 215-226 ◽  
Author(s):  
Fernanda R. C. Giachini ◽  
Victor V. Lima ◽  
Fernando P. Filgueira ◽  
Anne M. Dorrance ◽  
Maria Helena C. Carvalho ◽  
...  
Keyword(s):  
Sex Differences ◽  
Neutralizing Antibodies ◽  
Spontaneously Hypertensive Rats ◽  
Female Rats ◽  
Hypertensive Rats ◽  
Vascular Protection ◽  
Spontaneously Hypertensive ◽  
Female Sex Hormones ◽  
Impaired Control ◽  
Wistar Kyoto

Sex differences in Ca2+-dependent signalling and homoeostasis in the vasculature of hypertensive rats are well characterized. However, sex-related differences in SOCE (store-operated Ca2+ entry) have been minimally investigated. We hypothesized that vascular protection in females, compared with males, reflects decreased Ca2+ mobilization due to diminished activation of Orai1/STIM1 (stromal interaction molecule 1). In addition, we investigated whether ovariectomy in females affects the activation of the Orai1/STIM1 pathway. Endothelium-denuded aortic rings from male and female SHRSP (stroke-prone spontaneously hypertensive rats) and WKY (Wistar–Kyoto) rats and from OVX (ovariectomized) or sham female SHRSP and WKY rats were used to functionally evaluate Ca2+ influx-induced contractions. Compared with females, aorta from male SHRSP displayed: (i) increased contraction during the Ca2+-loading period; (ii) similar transient contraction during Ca2+ release from the intracellular stores; (iii) increased activation of STIM1 and Orai1, as shown by the blockade of STIM1 and Orai1 with neutralizing antibodies, which reversed the sex differences in contraction during the Ca2+-loading period; and (iv) increased expression of STIM1 and Orai1. Additionally, we found that aortas from OVX-SHRSP showed increased contraction during the Ca2+-loading period and increased Orai1 expression, but no changes in the SR (sarcoplasmic reticulum)-buffering capacity or STIM1 expression. These findings suggest that augmented activation of STIM1/Orai1 in aortas from male SHRSP represents a mechanism that contributes to sex-related impaired control of intracellular Ca2+ levels. Furthermore, female sex hormones may negatively modulate the STIM/Orai1 pathway, contributing to vascular protection observed in female rats.

scholarly journals Enhanced myogenic response in the afferent arteriole of spontaneously hypertensive rats

2010 ◽  
Vol 298 (6) ◽  
pp. H1769-H1775 ◽  
Author(s):  
YiLin Ren ◽  
Martin A. D'Ambrosio ◽  
Ruisheng Liu ◽  
Patrick J. Pagano ◽  
Jeffrey L. Garvin ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Perfusion Pressure ◽  
Intraluminal Pressure ◽  
Myogenic Response ◽  
Afferent Arteriole ◽  
Hypertensive Rats ◽  
Luminal Diameter ◽  
Spontaneously Hypertensive ◽  
Before And After ◽  
Wistar Kyoto

Spontaneously hypertensive rats (SHRs) have normal glomerular capillary pressure even though renal perfusion pressure is higher, suggesting that preglomerular vessels exhibit abnormally high resistance. This may be due to increased superoxide (O2−) production, which contributes to the vasoconstriction in hypertension. We tested the hypothesis that the myogenic response of the afferent arteriole (Af-Art) is exaggerated in SHRs because of increased levels of reactive oxygen species (ROS). Single Af-Arts were microdissected from kidneys of SHRs and Wistar-Kyoto (WKY) rats and microperfused in vitro. When perfusion pressure in the Af-Art was increased stepwise from 60 to 140 mmHg, the luminal diameter decreased by 8.4 ± 2.9% in WKY Af-Arts but fell by 29.3 ± 5.6% in SHR Af-Arts. To test whether ROS production is enhanced during myogenic response in SHRs, we measured chloromethyl-dichlorodihydrofluorescein diacetate acetyl ester (CM-H2DCFDA) florescence before and after increasing intraluminal pressure from 60 to 140 mmHg. Pressure-induced increases in ROS were fourfold greater in SHR Af-Arts compared with WKY Af-Arts (SHR, 48.0 ± 2.2%; and WKY, 12.2 ± 0.3%). To test whether O2− contributes to the myogenic response in SHRs, either the membrane-permeant O2− scavenger Tempol or the nox2-based NADPH oxidase (NOX2) inhibitor gp91 ds-tat were added to the Af-Art lumen and bath and the myogenic response was tested before and after treatment. Both Tempol (10−4 M) and gp91 ds-tat (10−5 M) significantly attenuated the pressure-induced constriction in SHR Af-Arts but not in WKY Af-Arts. We conclude that 1) pressure-induced constriction is exaggerated in SHR Af-Arts, 2) NOX2-derived O2− may contribute to the enhanced myogenic response, and 3) O2− exerts little influence on the myogenic response under normotensive conditions.

Daily exercise and gender influence postexercise cardiac autonomic responses in hypertensive rats

1997 ◽  
Vol 272 (3) ◽  
pp. H1412-H1418 ◽  
Author(s):  
Y. Chen ◽  
M. P. Chandler ◽  
S. E. DiCarlo
Keyword(s):  
Acute Exercise ◽  
Female Rats ◽  
Male Rats ◽  
Autonomic Response ◽  
Hypertensive Rats ◽  
Experimental Conditions ◽  
Autonomic Responses ◽  
Gender Influence ◽  
Single Bout ◽  
And Gender

The influence of daily spontaneous running (DSR) and gender on postexercise cardiac autonomic responses was examined in spontaneously hypertensive rats. Rats were weaned at 4-5 wk of age and were randomly assigned to a sedentary (7 males and 6 females) or DSR (7 males and 8 females) group. After 8 weeks of DSR or sedentary control, rats were chronically instrumented with arterial and venous catheters. After 5 days of recovery, cardiac sympathetic (ST) and parasympathetic tonus (PT) were determined (by the response of heart rate to receptor antagonists) on alternate days under two experimental conditions: no exercise and postexercise. After a single bout of dynamic treadmill exercise (12 m/min, 10% grade for 40 min) ST was reduced (P < 0.05) (male sedentary: no exercise 45 +/- 4 vs. postexercise 28 +/- 3 beats/min; female sedentary: no exercise 69 +/- 10 vs. postexercise 37 +/- 7 beats/ min). PT was also altered after exercise (male sedentary: no exercise -31 +/- 4 vs. postexercise -11 +/- 2 beats/min; female sedentary: no exercise -5 +/- 4 vs. postexercise 7 +/- 4 beats/min). After DSR, ST was reduced (male sedentary 45 +/- 4 vs. DSR 22 +/- 3 beats/min; female sedentary 69 +/- 10 vs. DSR 36 +/- 4 beats/min) (P < 0.05). Finally, male rats had a lower ST and higher PT than female rats. These results demonstrate that 1) ST was reduced after a single bout of dynamic exercise; 2) ST was reduced after DSR; 3) the autonomic response to acute exercise was attenuated after DSR; and 4) there was a gender influence on the cardiac autonomic function.

scholarly journals Estradiol increases salt intake in female normotensive and hypertensive rats

2002 ◽  
Vol 93 (2) ◽  
pp. 479-483 ◽  
Author(s):  
Eric Kensicki ◽  
Gail Dunphy ◽  
Daniel Ely
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Significant Positive Correlation ◽  
Salt Intake ◽  
Sodium Intake ◽  
Female Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Higher Doses ◽  
Sodium Consumption

The objective of this study was to examine whether or not estradiol (E2) alters sodium intake in hypertensive and normotensive female rats. It was hypothesized that higher doses of E2 would increase sodium consumption and that this response would be greater in spontaneously hypertensive rats (SHR) compared with Wistar Kyoto (WKY) rats. The study involved female SHR and WKY ( n = 12/group). All animals were ovariectomized. Six of twelve rats from each strain received three progressively larger doses of β-estradiol propionate (each dose lasting 2 wk), whereas the other six rats from each strain received sham implants. Blood E2 levels were measured by radioimmunoassay after each 2-wk period, allowing a 10-day washout period before the next E2 dose. Rats had access to 0.0, 0.5, 1.0, and 1.5% NaCl solutions to drink throughout the experiment. There was a significant positive correlation between sodium intake and plasma E2 ( r = 0.8, P < 0.001). Both strains avoided the 1.5% NaCl, and the increased sodium intake was achieved by an increase in consumption of the 0.5% NaCl. SHR females consumed more sodium than WKY females, which is similar to what has been observed in males of these strains. In conclusion, E2 was positively correlated with sodium intake in both strains of rat, with the hypertensive rats consuming more sodium than the normotensive rats.

Decreased in vitro responses to vasoconstrictors during gestation in normotensive and spontaneously hypertensive rats

1987 ◽  
Vol 65 (12) ◽  
pp. 2466-2471 ◽  
Author(s):  
G. Massicotte ◽  
J. St-Louis ◽  
A. Parent ◽  
E. L. Schiffrin
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Female Rats ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Pregnant Rats ◽  
Spontaneously Hypertensive ◽  
Vasoconstrictor Agents ◽  
Wistar Kyoto

We have investigated the in vitro vascular responses to vasoconstrictor agents in pregnant normotensive (Sprague–Dawley (SDR) and Wistar–Kyoto (WKR)) and spontaneously hypertensive rats (SHR) to measure the sensitivity and contractility of blood vessels of pregnant rats. In the perfused mesenteric vascular bed from rats on the 21st day of gestation, the concentration–response curves for the increase in perfusion pressure by arginine8-vasopressin and norepinephrine were displaced to the right by comparison to nonpregnant female rats when all strains of rats were considered together. The increase in EC50 to both agents in pregnant rats was from 1.3- to 2.7-fold in the mesenteric bed; SDR showed the highest increase in EC50, followed by SHR and WKR. No consistent effect was observed on the maximum response. Similar results were obtained in isolated portal veins for angiotensin II and norepinephrine, except that the increase in EC50 in pregnant rats was smaller in magnitude (from 1.0 to 1.7) and followed the same interstrain pattern. These data show that the decreased responsiveness to vasoconstrictor agents in pregnant rats observed in vitro is similar in normotensive and hypertensive rats and suggest that the factor(s) responsible for this effect is a phenomenon affecting vascular smooth muscle in both arteries and veins.

Corticosterone 6 beta-hydroxylation correlates with blood pressure in spontaneously hypertensive rats

1992 ◽  
Vol 262 (6) ◽  
pp. F927-F931 ◽  
Author(s):  
C. O. Watlington ◽  
L. B. Kramer ◽  
E. G. Schuetz ◽  
J. Zilai ◽  
W. M. Grogan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Selective Inhibitor ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Human Hypertension ◽  
Before And After ◽  
Wistar Kyoto ◽  
Cytochrome P 450

Evidence for increased glucocorticoid 6 beta-hydroxylation (enhanced family 3A cytochrome P-450 activity) is found in certain reversible forms of human hypertension. This association was investigated in the spontaneously hypertensive rat (SHR). The proportion of injected [3H]corticosterone excreted in urine as 6 beta-[3H]OH-corticosterone was four- to fivefold higher in SHR than in control Wistar-Kyoto rats, before and after development of overt hypertension. Both hypertension and 6 beta-hydroxylation were inhibited by troleandomycin (a selective inhibitor of family 3A cytochromes P-450), consistent with a role for increased steroid 6 beta-hydroxylation in the genesis of hypertension in the SHR.

scholarly journals Swimming Exercise Changes Hemodynamic Responses Evoked by Blockade of Excitatory Amino Receptors in the Rostral Ventrolateral Medulla in Spontaneously Hypertensive Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Cristiana A. Ogihara ◽  
Gerhardus H. M. Schoorlemmer ◽  
Maria de Fátima M. Lazari ◽  
Gisele Giannocco ◽  
Oswaldo U. Lopes ◽  
...  
Keyword(s):  
Mesenteric Artery ◽  
Spontaneously Hypertensive Rats ◽  
Rostral Ventrolateral Medulla ◽  
Swimming Exercise ◽  
Ventrolateral Medulla ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Before And After ◽  
Wistar Kyoto

Exercise training reduces sympathetic activity in hypertensive humans and rats. We hypothesized that the swimming exercise would change the neurotransmission in the rostral ventrolateral medulla (RVLM), a key region involved in sympathetic outflow, and hemodynamic control in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Bilateral injections of kynurenic acid (KYN) were carried out in the RVLM in sedentary- (S-) or exercised- (E-) SHR and WKY rats submitted to swimming for 6  weeks. Rats wereα-chloralose anesthetized and artificially ventilated, with Doppler flow probes around the lower abdominal aorta and superior mesenteric artery. Injections into the RVLM were made before and after i.v. L-NAME (nitric oxide synthase, NOS, inhibitor). Injections of KYN into the RVLM elicited a major vasodilation in the hindlimb more than in the mesenteric artery in E-SHR compared to S-SHR, but similar decrease in arterial pressure was observed in both groups. Injections of KYN into the RVLM after i.v. L-NAME attenuated the hindlimb vasodilation evoked by KYN and increased the mesenteric vasodilation in E-SHR. Swimming exercise can enhance the hindlimb vasodilation mediated by peripheral NO release, reducing the activation of neurons with EAA receptors in the RVLM in SHR.

Enhanced sympathetic reactivity to glutamate stimulation in medulla oblongata of spontaneously hypertensive rats

1995 ◽  
Vol 268 (4) ◽  
pp. H1499-H1509 ◽  
Author(s):  
T. L. Yang ◽  
C. Y. Chai ◽  
C. T. Yen
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Significant Difference ◽  
Baseline Adjustment ◽  
Before And After ◽  
Threshold Doses ◽  
Wistar Kyoto ◽  
Alpha Chloralose ◽  
Renal Sympathetic

The distribution and reactivity of vasomotor sites in the ventrolateral (VLM) and dorsomedial medulla (DMM) of stroke-prone spontaneously hypertensive rats (SHRSP), spontaneously hypertensive rats (SHR), and Wistar-Kyoto rats (WKY) were compared. Rats were anesthetized with alpha-chloralose and urethan. Baroreceptor denervation and vagotomy were performed. L-Glutamate (Glu, 10 mM, 30 nl) was microinjected into the DMM or VLM to identify vasoactive sites. The extent and the patterns of distribution of these sites in the three strains of rats were similar. The dose-response curve of the vasoactive site was studied with 1–500 pmol of Glu. The maximum responses of blood pressure and renal sympathetic activity were larger and threshold doses of Glu were lower in hypertensive rats. The significance of the differences among the strains was analyzed before and after adjustment for baseline pressure or activity. Most of the differences were statistically significant before baseline adjustment. After baseline adjustment, many differences between the SHRSP and the WKY remained significant. However, the only significant difference detected between the SHR and the WKY was the threshold dose for eliciting renal sympathetic change in the caudal VLM. These results suggest that there may be a general increase in excitability of the vasomotor neurons in the medulla of the hypertensive rats.

Intranephron PGE2 production in stroke-prone spontaneously hypertensive rats

1990 ◽  
Vol 258 (4) ◽  
pp. H987-H993 ◽  
Author(s):  
F. Takemoto ◽  
A. Miyanoshita ◽  
K. Shimamura ◽  
S. Sunano ◽  
H. Endou
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Collecting Duct ◽  
Pge2 Production ◽  
Male Rats ◽  
Ionophore A23187 ◽  
Hypertensive Rats ◽  
Adult Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Collecting Tubules

To investigate whether intranephron prostaglandin E2 (PGE2) production in stroke-prone spontaneously hypertensive rats (SHRSP) differs from that in Wistar-Kyoto rats (WKY), we measured PGE2 accumulation rates in microdissected nephron segments from 4- to 6- and 12- to 14-wk-old male rats by radioimmunoassay. In both young and adult WKY, PGE2 accumulation was highest in the papillary collecting duct (PCD) and outer medullary and cortical collecting tubules, intermediate in the glomerulus (Glm), medullary and cortical thick ascending limbs of Henle's loop, and distal tubule, and negligible in the proximal tubule. PGE2 accumulation in adult WKY was severalfold higher than that in young WKY. PGE2 accumulation in adult and prehypertensive young SHRSP was significantly lower than that of respective WKY in most segments, whereas urinary PGE2 excretion was significantly higher in SHRSP than in age-matched WKY. Plasma arginine vasopressin concentrations in adult SHRSP were significantly higher than in WKY. PGE2 accumulation stimulated by 5 microM arachidonic acid was significantly lower in SHRSP than in WKY in most segments of young rats but was lower only in Glm and PCD of adult rats. PGE2 accumulation stimulated by 2 microM Ca2+ ionophore A23187 was significantly lower in most segments of adult and young SHRSP. These results indicate that a decrease in renal tubular PGE2 productive activities in SHRSP might not be caused by secondary adaptation to hypertension.

Use of nonlinear methods to assess effects of clonidine on blood pressure in spontaneously hypertensive rats

1998 ◽  
Vol 84 (5) ◽  
pp. 1795-1800 ◽  
Author(s):  
Denis Mestivier ◽  
Hubert Dabiré ◽  
Michel Safar ◽  
Nguyen Phong Chau
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Recurrence Plot ◽  
Hypertensive Rats ◽  
Nonlinear Methods ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Before And After ◽  
Pressure Dynamics ◽  
Wistar Kyoto

In spontaneously hypertensive rats (SHR), chronic infusion of clonidine failed to decrease blood pressure and blood pressure variability. We used nonlinear methods to get a deeper insight on the effects of clonidine on blood pressure dynamics. For 24 h and 4 wk, clonidine (0.1 mg ⋅ kg−1 ⋅ day−1sc) was infused by minipumps in the conscious SHRs, and, for comparison, a vehicle was infused in SHRs and in Wistar-Kyoto rats. Blood pressure was recorded for 30 min before and after treatments. We used the Lyapunov exponent, approximated by the inverse of the l max index derived from the recurrence plot method, to characterize nonlinear dynamics. Before treatment, l max index of blood pressure was lower ( P < 0.01) in the SHRs than in the Wistar-Kyoto rats. Clonidine significantly increased l max( P < 0.01) to the level observed in normotensive rats, at 24 h and up to 4 wk after infusion. We conclude that clonidine has a significant chronic effect on blood pressure dynamics, as evidenced by nonlinear methods. Our study also suggests that the mechanisms governing blood pressure variations are nonlinear.

Sign in / Sign up

Export Citation Format

Share Document