Soleus muscle contractile properties in hypertensive rats

1994 ◽  
Vol 267 (3) ◽  
pp. R735-R739 ◽  
Author(s):  
S. D. Gray ◽  
R. C. Carlsen ◽  
J. Deng
Keyword(s):  
Blood Pressure ◽  
High Blood Pressure ◽  
Soleus Muscle ◽  
Spontaneously Hypertensive Rat ◽  
Fatigue Properties ◽  
Hypertensive Rats ◽  
Tension Development ◽  
Spontaneously Hypertensive ◽  
Adequate Blood Supply ◽  
Wistar Kyoto

Three types of hypertensive rats, and their normotensive controls, were assessed to determine the effects of high blood pressure on the contractile and fatigue properties of the soleus muscle. Spontaneously hypertensive rat (SHR) soleus developed less contractile force and fatigued more rapidly than normotensive Wistar-Kyoto (WKY) controls. In contrast, normotensive Wistar and Wistar-1 kidney/1 renal clip hypertensives were similar in their responses, and Dahl salt-sensitive hypertensives and Dahl salt-resistant controls also did not exhibit any significant differences in tension development or endurance. The results suggest that the decreased ability to develop force and maintain it during stimulation may not be directly related to the high blood pressure in SHR. It may instead be related to a gene defect that cosegregates with the loci responsible for the rise in blood pressure. The reduced endurance in SHR may be associated with an increased accumulation of K+ in the muscle during contraction, which decreases performance. It may also decrease the ability of the vessels to dilate during muscle contraction, preventing maintenance of an adequate blood supply.

Cell Membrane Microviscosity and Ca2+-Mg2+-ATPase Activity do Not Contribute to Hypertension in the Spontaneously Hypertensive Rat Model

1993 ◽  
Vol 85 (5) ◽  
pp. 585-591 ◽  
Author(s):  
Robert I Norman ◽  
Navtej Achall
Keyword(s):  
Blood Pressure ◽  
Atpase Activity ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Hypertensive Rats ◽  
Membrane Microviscosity ◽  
Spontaneously Hypertensive ◽  
Blood Pressures ◽  
Wistar Kyoto ◽  
Spontaneously Hypertensive Rat Model

1. The relationships between systolic blood pressure and altered erythrocyte Ca2+-Mg2+-ATPase activity and membrane microviscosity were assessed in membranes prepared from 20-week-old female Wistar-Kyoto normotensive and spontaneously hypertensive rats obtained from two different sources (Charles River and Harlan OLAC) and a second filial (F2) generation derived from a cross between Wistar-Kyoto rats and spontaneously hypertensive rats from one source (Charles River). 2. Spontaneously hypertensive rats from both sources had systolic blood pressures significantly higher than those of Wistar-Kyoto animals (P <0.05; 151 + 4 and 110 + 3 mmHg, Charles River; 155 + 4 and 122 + 4 mmHg, Harlan OLAC). The systolic blood pressures for the F2 rat population ranged between 73 and 168 mmHg. 3. Ca2+-Mg2+-ATPase activity was measured as ATP-dependent 45Ca2+ uptake into inside-out vesicles and microviscosity assessed by the measurement of polarization anisotropy of membrane incorporated fluorescent probes including 1,6-diphenyl-1,3,5-hexatriene, trimethylamino-1,6-diphenyl-1,3,5-hexatriene and a series of anthroyloxy fatty acids. 4. Contrary to previous studies, no relationship between adult systolic blood pressure and erythrocyte Ca2+-Mg2+-ATPase activity or general or localized membrane microviscosity was indicated by the comparison of spontaneously hypertensive and Wistar-Kyoto animals or in the analysis of the F2 rat population. 5. These results suggest that Ca2+-Mg2+-ATPase activity and membrane microviscosity are causally unrelated to hypertension in these animals. On the assumption that biophysical properties of the erythrocyte membrane reflect those of smooth muscle, our results suggest that membrane alteration does not play a significant role in the pathogenesis of hypertension in the spontaneously hypertensive rat model.

scholarly journals Chronic NO Restriction in Hypertensive Rats Increases Abdominal but Not Thoracic Aortic Intrinsic Stiffness via an Augmentation in Profibrotic Materials

2019 ◽  
Vol 2019 ◽  
pp. 1-11
Author(s):  
George Lindesay ◽  
Yvonnick Bézie ◽  
Christophe Ragonnet ◽  
Véronique Duchatelle ◽  
Marc Isabelle ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rat ◽  
Dynamic Properties ◽  
Stiffness Index ◽  
Operating Pressure ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Spontaneously Hypertensive Rat Model

The spontaneously hypertensive rat model with reduced NO synthesis (SHRLN) shares features with aging and hypertension in humans, among other a severe aortic stiffening. The present in vivo study aimed to compare thoracic (TA) and abdominal (AA) aortic stiffness in the SHRLN (treated 5 weeks with L-NAME), SHR, and normotensive Wistar Kyoto (WKY). Dynamic properties of TA and AA were measured in the same rats, using echotracking recording of aortic diameter coupled with blood pressure (BP). Measurements were performed first at operating BP and then after BP reduction in hypertensive rats, thus in isobaric conditions. Histological staining and immunohistochemistry were used for structural analysis at both sites. At operating pressure, BP and pulse pressure (PP) were higher in SHRLN compared with SHR. Stiffness index was also increased and distensibility decreased in both TA and AA in SHRLN. At WKY-matched blood pressure, isobaric AA parameters remained specifically altered in SHRLN, whereas TA recovered to values identical to WKYs. Collagen, fibronectin, α5-selectin, and FAK were increased in SHRLN compared with SHR or WKY. Nevertheless, only the strong accumulations of fibronectin and collagen at the AA site in SHRLN were associated with intrinsic stiffening. In conclusion, we confirm that NO restriction associated with hypertension induces a severe pathological phenotype and shows that L-NAME induced stiffening is more pronounced in AA than in TA as a result of greater fibrosis.

Effect of chronic blood pressure reduction on soleus muscle contractile properties in spontaneously hypertensive rats

1994 ◽  
Vol 267 (3) ◽  
pp. R740-R746
Author(s):  
S. D. Gray ◽  
R. C. Carlsen ◽  
R. Atherley
Keyword(s):  
Blood Pressure ◽  
Fatigue Resistance ◽  
Soleus Muscle ◽  
Spontaneously Hypertensive Rats ◽  
Blood Pressure Reduction ◽  
Contractile Force ◽  
Force Generation ◽  
Fatigue Properties ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Soleus muscle in Wistar-Kyoto rats (WKY), as well as in most normotensive mammals, is highly fatigue resistant. In 6-mo-old spontaneously hypertensive rats (SHR), however, soleus muscle generates less specific force and experiences a more rapid rate of fatigue than in age-matched WKY. The present experiments tested the hypothesis that antihypertensive treatment with hydralazine or amlodipine would shift the contractile force and fatigue resistance profile of SHR soleus toward that which characterizes WKY. Hydralazine was given via the drinking water (100 mg/l) and amlodipine via the food (1 g/4 kg rat chow) to two separate groups of animals, starting at the age of 16 wk. At 24-26 wk of age soleus twitch and tetanic force generation and the rate of fatigue were evaluated during a 4-min period of repetitive stimulation. Although both hydralazine and amlodipine lowered blood pressure, they had different effects on muscle function. Hydralazine decreased force generation in both WKY and SHR at all stimulation frequencies; it did not change the fatigue properties of SHR but made WKY soleus less fatigue resistant. Amlodipine, on the other hand, increased contractile force in both WKY and SHR and increased fatigue resistance in SHR. Amlodipine is a dihydropyridine that blocks L-type channels, thereby preventing entry of Ca2+ into the muscle. We suggest that Ca2+ entry during activity stimulates Ca-activated K+ efflux in SHR and adds to the extracellular load of K+. Increased extracellular K+ can in turn depress contractile performance.

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.

Vasopressin withdrawal produces hypotension in the spontaneously hypertensive rat

1985 ◽  
Vol 249 (1) ◽  
pp. H193-H197 ◽  
Author(s):  
E. K. Chiu ◽  
J. R. McNeill
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Pressor Agent

In spontaneously hypertensive rats (SHR) and their normotensive Wistar-Kyoto controls (WKY), prolonged intravenous infusions of either arginine vasopressin (AVP, 8 mU X kg-1 X min-1) or phenylephrine (PE, 20 nmol X kg-1 X min-1) resulted in similar rises in arterial pressure. Heart rate fell greatly in the WKY but not in the SHR. Withdrawal of the PE infusion resulted in moderate decreases in blood pressure and increases in heart rate; these responses were similar in SHR and WKY. At 5 h after PE withdrawal, blood pressure and heart rate returned to basal values. In contrast, withdrawal of the AVP infusion was associated with greater falls in blood pressure and rises in heart rate. Blood pressure and heart rate in both the SHR and the WKY at 5 h after AVP were significantly different from their respective basal values. The effects of AVP withdrawal on either blood pressure or heart rate were significantly greater in the SHR than in the WKY. At 5 h after the withdrawal of AVP, blood pressure in the SHR was reduced to normotensive levels. These results suggest that the withdrawal effect was specific to AVP, was more marked in the SHR, and might not result from only the rise in blood pressure seen during the intravenous infusion of the pressor agent.

Intrathecal PACAP-38 causes increases in sympathetic nerve activity and heart rate but not blood pressure in the spontaneously hypertensive rat

2011 ◽  
Vol 300 (1) ◽  
pp. H214-H222 ◽  
Author(s):  
Melissa M. J. Farnham ◽  
Melissa A. Inglott ◽  
Paul M. Pilowsky
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spontaneously Hypertensive Rat ◽  
Sympathetic Tone ◽  
Ventrolateral Medulla ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Wistar Kyoto ◽  
Intrathecal Infusion

The rostral ventrolateral medulla contains presympathetic neurons that project monosynaptically to sympathetic preganglionic neurons (SPN) in the spinal cord and are essential for the tonic and reflex control of the cardiovascular system. SPN directly innervate the adrenal medulla and, via postganglionic axons, affect the heart, kidneys, and blood vessels to alter sympathetic outflow and hence blood pressure. Over 80% of bulbospinal, catecholaminergic (C1) neurons contain pituitary adenylate cyclase-activating polypeptide (PACAP) mRNA. Activation of PACAP receptors with intrathecal infusion of PACAP-38 causes a robust, prolonged elevation in sympathetic tone. Given that a common feature of most forms of hypertension is elevated sympathetic tone, this study aimed to determine in the spontaneously hypertensive rat (SHR) and the Wistar Kyoto rat (normotensive control) 1) the proportion of C1 neurons containing PACAP mRNA and 2) responsiveness to intrathecal PACAP-38. We further investigated whether intrathecal infusion of the PACAP antagonist, PACAP(6–38), reduces the hypertension in the SHR. The principal findings are that 1) the proportion of PACAP mRNA-containing C1 neurons is not different between normotensive and hypertensive rats, 2) intrathecal PACAP-38 causes a strain-dependent, sustained sympathoexcitation and tachycardia with variable effects on mean arterial pressure in normotensive and hypertensive rats, and 3) PACAP(6–38) effectively attenuated the effects of intrathecal PACAP-38, but had no effect alone, on any baseline variables. This finding indicates that PACAP-38 is not tonically released in the spinal cord of rats. A role for PACAP in hypertension in conscious rats remains to be determined.

The effect of prolonged infusion and withdrawal of angiotensin II in the spontaneously hypertensive rat

1986 ◽  
Vol 64 (6) ◽  
pp. 748-750 ◽  
Author(s):  
Edward K. Y. Chiu ◽  
J. Robert McNeill
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Hypertensive Rats ◽  
Prolonged Infusion ◽  
Spontaneously Hypertensive ◽  
Control Value ◽  
Arterial Blood ◽  
Wistar Kyoto

In spontaneously hypertensive rats (SHR) and their normotensive Wistar–Kyoto controls (WKY), prolonged intravenous administration of angiotensin II (AII, 0.2 μg∙kg−1∙min−1 for 3 h) resulted in similar increases in arterial blood pressure. Heart rate decreased in WKY and increased in SHR. At the end of the infusion, blood pressure dropped substantially in SHR, but not in WKY: at 5 h after AII withdrawal, blood pressure in SHR had fallen from a control value of 172 ± 3.3 to 146 ± 3.9 mmHg (p < 0.01), whereas pressure in WKY had fallen from 116 ± 3.0 to 107 ± 4.2 mmHg (statistically non significant). Thus, pressure at 5 h after AII withdrawal was still substantially higher (p < 0.01) in the SHR than in the WKY. The results demonstrate that the fall in blood pressure following withdrawal of a prolonged infusion of AII in SHR is much less than that reported to occur following withdrawal of a prolonged infusion of vasopressin (AVP) in SHR.

Is Arterial Media Hypertrophy in Spontaneously Hypertensive Rats a Consequence of or a Cause for Hypertension?

1980 ◽  
Vol 59 (s6) ◽  
pp. 331s-333s ◽  
Author(s):  
K. J. Henrichs ◽  
T.H. Unger ◽  
K. H. Berecek ◽  
D. Ganten
Keyword(s):  
Blood Pressure ◽  
High Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Structural Changes ◽  
Peripheral Resistance ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
The Media ◽  
Wistar Kyoto ◽  
Genetically Determined

1. The increased peripheral resistance observed in established hypertension has been attributed to structural changes in the resistance vessels, which are considered to be due mainly to medial hypertrophy. This study was undertaken to examine the possiblity that structural changes in the arterial bed are genetically determined and may be causative factors in the development of high blood pressure in the spontaneously hypertensive rat. 2. The wall dimensions of aorta, renal artery and intrarenal arteries down to a distended diameter of 35 μm were studied: (a) in 14-week-old spontaneously hypertensive rats; (b) in age- and sex-matched spontaneously hypertensive rats which had been treated with captopril for two generations and had been normotensive during their complete life span; (c) in normotensive Wistar-Kyoto control rats. 3. Cross-sectional areas of the media were increased in the hypertensive rats in comparison with ‘normotensive spontaneously hypertensive rats’ and Wistar-Kyoto rats. Increased numbers of smooth muscle cells were found in the major arteries of hypertensive animals. 4. These results indicate that hypertrophy of the media is a consequence of high blood pressure rather than a genetically determined pathogenetic factor for the development of hypertension in spontaneously hypertensive rats.

scholarly journals Metabolic Mapping in the Sympathetic Ganglia and Brain of the Spontaneously Hypertensive Rat

1983 ◽  
Vol 3 (4) ◽  
pp. 460-467 ◽  
Author(s):  
Massako Kadekaro ◽  
Helen E. Savaki ◽  
Francis A. Kutyna ◽  
Leslie Davidsen ◽  
Louis Sokoloff
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Glucose Utilization ◽  
Spontaneously Hypertensive Rat ◽  
Sympathetic Ganglia ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Arterial Blood ◽  
Cervical Ganglia ◽  
Wistar Kyoto

Local rates of glucose utilization in the superior cervical, cardiac, and coeliac ganglia were measured by means of the autoradiographic 2-deoxy-d-[14C]glucose method in male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY), 32–34, 46–48, and 78–87 days old. Brain glucose utilization was examined in 78–87-day-old SHR and WKY. At 32–34 days (at which time mean arterial blood pressure was normal and similar in both groups of rats), the rates of glucose utilization of all three sympathetic ganglia were the same in both groups. At 46–48 days, despite the fact that blood pressure had risen significantly in SHR (mean ± SEM, 136 ± 3 mm Hg, n = 5, compared to 113 ± 3 mm Hg, n = 5, in the control WKY), glucose utilization was decreased in the cardiac and coeliac ganglia but not in the superior cervical ganglia of the SHR. At 78–87 days, glucose utilization was reduced in all the sympathetic ganglia of the hypertensive rats. These results suggest that the sympathetic system is less active in SHR and indicate that hyperactivity of the sympathetic nervous system is not part of the mechanism of the hypertension. Of 44 structures examined in the central nervous system, only the external cuneate, vestibular, and fastigial nuclei of the SHR exhibited increased rates of glucose utilization, and no changes were found in any of the other structures. These increases are probably not related to the origin or maintenance of the hypertension, inasmuch as lesioning of the vestibular or fastigial nuclei did not decrease blood pressure in the SHR.

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