Clonidine fails to reduce pressor responsiveness of conscious spontaneously hypertensive rats to vasopressin

1986 ◽  
Vol 64 (3) ◽  
pp. 284-289 ◽  
Author(s):  
Sunil Datar ◽  
William H. Laverty ◽  
J. Robert McNeill
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Reflex Activity ◽  
Unexpected Finding ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto ◽  
Shr And Wky Rats

Pressor responses and heart rate responses to intravenous injections (3.5–50.0 pmol/kg) of arginine vasopressin (AVP) were recorded in saline- and clonidine-treated spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. Clonidine (20 μg/kg, i. v.) caused a marked fall of arterial pressure in SHR but not in WKY rats so that, 20 min after the injection of the α2-adrenoceptor agonist, arterial pressure was similar in the two strains of rats. The curve expressing the relationship between the dose of AVP and the increase of arterial pressure for saline-treated SHR was positioned to the left of that for saline-treated WKY rats. This enhanced pressor responsiveness of SHR to AVP may have been related to impaired reflex activity since heart rate fell much less in SHR than in WKY rats for a given elevation in pressure. Pressure responses to AVP were augmented by clonidine in both SHR and WKY rats so that, similar to saline-treated rats, pressor responsiveness to the peptide was still greater in SHR. Heart rate responses to AVP were not altered significantly by clonidine. The results indicate that clonidine fails to enhance reflex activity and reduce pressor responsiveness of SHR to AVP. The increased pressor responsiveness of both SHR and WKY rats to AVP following clonidine was an unexpected finding and may be related to a peripheral interaction between α-adrenergic agonists and AVP.

scholarly journals Exercise changes regional vascular control by commissural NTS in spontaneously hypertensive rats

2010 ◽  
Vol 299 (1) ◽  
pp. R291-R297 ◽  
Author(s):  
Cristiana A. Ogihara ◽  
Gerhardus H. M. Schoorlemmer ◽  
Adriana C. Levada ◽  
Tania C. Pithon-Curi ◽  
Rui Curi ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
The Body ◽  
Swimming Exercise ◽  
Exercise Session ◽  
Hypertensive Rats ◽  
Vascular Control ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto

Inhibition of the commissural nucleus of the solitary tract (commNTS) induces a fall in sympathetic nerve activity and blood pressure in spontaneously hypertensive rats (SHR), which suggests that this subnucleus of the NTS is a source of sympathoexcitation. Exercise training reduces sympathetic activity and arterial pressure. The purpose of the present study was to investigate whether the swimming exercise can modify the regional vascular responses evoked by inhibition of the commNTS neurons in SHR and normotensive Wistar-Kyoto (WKY) rats. Exercise consisted of swimming, 1 h/day, 5 days/wk for 6 wks, with a load of 2% of the body weight. The day after the last exercise session, the rats were anesthetized with intravenous α-chloralose, tracheostomized, and artificially ventilated. The femoral artery was cannulated for mean arterial pressure (MAP) and heart rate recordings, and Doppler flow probes were placed around the lower abdominal aorta and superior mesenteric artery. Microinjection of 50 mM GABA into the commNTS caused similar reductions in MAP in swimming and sedentary SHR (−25 ± 6 and −30 ± 5 mmHg, respectively), but hindlimb vascular conductance increased twofold in exercised vs. sedentary SHR (54 ± 8 vs. 24 ± 5%). GABA into the commNTS caused smaller reductions in MAP in swimming and sedentary WKY rats (−20 ± 4 and −16 ± 2 mmHg). Hindlimb conductance increased fourfold in exercised vs. sedentary WKY rats (75 ± 2% vs. 19 ± 3%). Therefore, our data suggest that the swimming exercise induced changes in commNTS neurons, as shown by a greater enhancement of hindlimb vasodilatation in WKY vs. SHR rats in response to GABAergic inhibition of these neurons.

Methionine-enkephalin and vasopressin in SHR: effects of dehydration

1986 ◽  
Vol 250 (6) ◽  
pp. R1007-R1013
Author(s):  
K. Ota ◽  
L. Share ◽  
J. T. Crofton ◽  
D. P. Brooks
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Posterior Pituitary ◽  
Hypertensive Rats ◽  
Methionine Enkephalin ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Wistar Kyoto ◽  
Shr And Wky Rats

Enkephalins are found in the posterior pituitary, can alter vasopressin secretion, and have greater pressor effects in spontaneously hypertensive rats (SHR) than in Wistar-Kyoto (WKY) rats. Measurement of the plasma methionine-enkephalin concentration (PMet-Enk) has provided equivocal results in humans and has not been reported in rats. We have developed a highly specific and sensitive Met-Enk radioimmunoassay and determined that Met-Enk circulates in rats but that PMet-Enk is no different between SHR and WKY rats (7.6 +/- 0.8 and 9.2 +/- 0.8 pg/ml, respectively). Water deprivation for 48 h increased the plasma vasopressin concentration (PADH) and 24-h urinary vasopressin excretion (UADHV) in SHR and WKY rats, but PMet-Enk was not altered. There were no differences in PADH and UADHV between SHR and WKY rats in either the euhydrated or dehydrated state. These results suggest that it is unlikely that circulating Met-Enk contributes importantly to the maintenance of hypertension in SHR. There was also no evidence for a greater secretion of vasopressin in SHR than in WKY rats, in contrast to previous reports.

Aortic stiffness and pulse pressure amplification in Wistar-Kyoto and spontaneously hypertensive rats

2007 ◽  
Vol 292 (5) ◽  
pp. H2506-H2512 ◽  
Author(s):  
Emmanuel Cosson ◽  
Monique Herisse ◽  
Dominique Laude ◽  
Frédérique Thomas ◽  
Paul Valensi ◽  
...  
Keyword(s):  
Heart Rate ◽  
Body Weight ◽  
Aortic Stiffness ◽  
Spontaneously Hypertensive Rats ◽  
Age Effect ◽  
Strain Effect ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto

In humans, increased body weight and arterial stiffness are significantly associated, independently of blood pressure (BP) level. The finding was never investigated in rodents devoid of metabolic disorders as spontaneously hypertensive rats (SHR). Using simultaneous catheterization of proximal and distal aorta, we measured body weight, intra-arterial BP, heart rate and their variability (spectral analysis), aortic pulse wave velocity (PWV), and systolic and pulse pressure (PP) amplifications in unrestrained conscious Wistar-Kyoto (WKY) rats and SHR between 6 and 24 wk of age. Aortic proximal systolic and diastolic pressure, PP, and mean BP were significantly higher in SHR than in WKY rats and increased significantly with age (with the exception of PP). PP amplification increased with age but did not differ between strains. PWV was significantly associated with heart rate variability. PWV was significantly higher (via two-way variance analysis) in SHR than in WKY rats (strain effect) and increased markedly with age in both strains (age effect). Adjustment of PWV to mean BP attenuated markedly both the age and the strain effects. After adjustment for body weight, either alone or associated with mean BP, the age effect was not more significant, but the strain effect was markedly enhanced. In conscious unanesthetized SHR and WKY rats, aortic stiffness is consistently associated with body weight independent of age and mean BP. An intervention study should consider in the objectives systolic BP and PP amplifications measured in conscious animals, central control of body weight, and autonomic nervous system.

Effects of dietary sodium on central and peripheral ouabain-like activity in spontaneously hypertensive rats

1993 ◽  
Vol 264 (6) ◽  
pp. H2051-H2055 ◽  
Author(s):  
F. H. Leenen ◽  
E. Harmsen ◽  
H. Yu ◽  
C. Ou
Keyword(s):  
Left Ventricle ◽  
Sympathetic Activity ◽  
Spontaneously Hypertensive Rats ◽  
Dietary Sodium ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto ◽  
Later Phase ◽  
Shr And Wky Rats

High dietary Na+ intake enhances pressor and sympathoexcitatory responses in spontaneously hypertensive rats (SHR) but not Wistar-Kyoto (WKY) rats. To evaluate the possible contribution of central ouabain-like activity (OLA), brain and peripheral OLA was assessed in SHR vs. WKY rats at 4 wk of age and after 2 and 4 wk of high vs. control Na+ intake started at 4 wk of age. In SHR, hypertension developed with maturation and was exacerbated by high Na+ intake. With control Na+ intake, SHR showed higher OLA at 4, 6, and 8 wk of age in the pituitary and hypothalamus and also by 8 wk in the adrenals and left ventricle but not in plasma. High Na+ intake increased OLA in all tissues examined in both WKY rats and SHR. After 2 wk on high Na+, only OLA in hypothalamus and pituitary was higher in SHR vs. WKY rats; after 4 wk on high Na+, peripheral (i.e., adrenals, left ventricle, and plasma) OLA was also higher. These results indicate that in SHR the development of hypertension is associated early on with increases in central OLA and in a later phase with increases in peripheral OLA as well. High Na+ intake increases OLA in both SHR and WKY rats, but the higher OLA may affect sympathetic activity and blood pressure only in SHR.

Insulin sensitivity and hemodynamic responses to insulin in Wistar-Kyoto and spontaneously hypertensive rats

1996 ◽  
Vol 271 (4) ◽  
pp. E658-E668 ◽  
Author(s):  
M. Pitre ◽  
A. Nadeau ◽  
H. Bachelard
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Insulin Sensitivity ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Hemodynamic Responses ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Vascular Beds ◽  
Wistar Kyoto

The insulin-mediated vasodilator effect has been proposed as an important physiological determinant of insulin action on glucose disposal in normotensive humans. The present study was designed to further examine the acute regional hemodynamic effects of insulin in different vascular beds and to explore the relationships between insulin vascular effects and insulin sensitivity during euglycemic hyperinsulinemic clamps in conscious normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The rats were instrumented with intravascular catheters and pulsed Doppler flow probes to measure blood pressure, heart rate, and regional blood flows. In WKY rats, the euglycemic infusion of insulin (4 and 16 mU.kg-1.min-1) causes vasodilations in renal and hindquarter vascular beds but no changes in mean blood pressure, heart rate, or superior mesenteric vascular conductance. In contrast, in SHR, the same doses of insulin produce vasoconstrictions in superior mesenteric and hindquarter vascular beds and, at high doses, increase blood pressure. Moreover, at the lower dose of insulin tested, we found a reduction in the insulin sensitivity index in the SHR compared with the WKY rats. The present findings provide further evidence for an association between insulin sensitivity and insulin-mediated hemodynamic responses.

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.

Norepinephrine concentration in kidneys of normotensive Wistar–Kyoto and spontaneously hypertensive rats

1979 ◽  
Vol 57 (4) ◽  
pp. 438-441 ◽  
Author(s):  
P. J. Stuart ◽  
R. L. Kline ◽  
P. F. Mercer
Keyword(s):  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Norepinephrine Concentration ◽  
The Difference ◽  
Wistar Kyoto

Renal norepinephrine (NE) concentration was measured in normotensive Wistar–Kyoto (WKY) and spontaneously hypertensive rats (SHR) at 7, 9, 11, and 13 weeks of age. Although the weight of kidneys was similar in the two strains of rats, renal NE concentration was significantly lower in SHR at all ages (147 ± 9 to 175 ± 13 ng/g for SHR, and 216 ± 8 to 262 ± 17 ng/g for WKY rats). The difference in renal NE concentration during this time of rapidly-increasing arterial pressure in the SHR suggests that renal NE may in some way be related to the development of hypertension.

scholarly journals Duration of Electrically Induced Atrial Fibrillation Is Augmented by High Voltage of Stimulus with Higher Blood Pressure in Hypertensive Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Tomomi Nagayama ◽  
Yoshitaka Hirooka ◽  
Akiko Chishaki ◽  
Masao Takemoto ◽  
Yasushi Mukai ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Blood Pressure ◽  
Arterial Pressure ◽  
High Voltage ◽  
Spontaneously Hypertensive Rats ◽  
Low Voltage ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Stimulus ◽  
Wistar Kyoto

Objective.Many previous clinical studies have suggested that atrial fibrillation (AF) is closely associated with hypertension. However, the benefits of antihypertensive therapy on AF are still inconsistent, and it is necessary to explore the factors augmenting AF in hypertensive rats. The aim of the present study was to investigate the correlation between arterial pressure or voltage stimulus and to the duration of electrically induced AF in normotensive or hypertensive rats.Methods.AF was reproducibly induced by transesophageal atrial burst pacing in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). We did the burst pacing at high (20 V) or low (5 V) voltage.Results.Duration of AF did not correlate with systolic blood pressure (SBP) and stimulus voltage in WKY. However, only in SHR, duration of AF with high stimulus voltage significantly correlated with SBP and was significantly longer in high than in low voltage stimulus.Discussion and Conclusion.Duration of AF is augmented by high voltage stimulus with higher blood pressure in SHR.

Functional and structural changes with hypoxia in pulmonary circulation of spontaneously hypertensive rats

1994 ◽  
Vol 77 (3) ◽  
pp. 1101-1107 ◽  
Author(s):  
S. P. Janssens ◽  
B. T. Thompson ◽  
C. R. Spence ◽  
C. A. Hales
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Vascular Remodeling ◽  
Spontaneously Hypertensive Rats ◽  
Structural Changes ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Chronic hypoxic pulmonary hypertension involves both vasoconstriction and vascular remodeling. Spontaneously hypertensive rats (SHR) have an increased systemic vascular resistance and a greater responsiveness to constricting stimuli. We hypothesized that, in contrast to age-matched normotensive Wistar-Kyoto rats (WKY), SHR also display spontaneous pulmonary hypertension in normoxia and increased vascular response to acute and chronic hypoxia. Baseline mean pulmonary arterial pressure (PAP) and total pulmonary resistance (TPR) were higher in SHR than in WKY. With acute hypoxia (10% O2 for 15 min), PAP increased to the same extent in SHR and WKY and cardiac output (CO) was unchanged in WKY but increased in SHR. Thus, the rise in PAP in the SHR might be accounted for by the rise in CO, as TPR did not rise, but not that in the WKY, as TPR increased. After 12 days in hypoxia (10% O2), mean arterial pressure was unchanged in WKY but decreased significantly in SHR without a change in CO. PAP increased by 59% in SHR and 54% in WKY when the rats were taken from the hypoxic chamber for 1 h. Acute hypoxic challenge caused a further increase in PAP only in WKY. Medial wall thickness of alveolar duct and terminal bronchial vessels was similar in WKY and SHR after chronic hypoxia. We conclude that SHR exhibit mild baseline pulmonary hypertension in normoxia and that chronic hypoxia does not produce a disproportionate increase in SHR pulmonary vascular remodeling and pulmonary hypertension.

Vasopressin V2 receptor enhances gain of baroreflex in conscious spontaneously hypertensive rats

1999 ◽  
Vol 276 (3) ◽  
pp. R872-R879 ◽  
Author(s):  
Donella B. Sampey ◽  
Louise M. Burrell ◽  
Robert E. Widdop
Keyword(s):  
Receptor Antagonist ◽  
Spontaneously Hypertensive Rats ◽  
Pressor Response ◽  
Receptor Subtype ◽  
Hypertensive Rats ◽  
Receptor Antagonists ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Baroreflex Function ◽  
Shr And Wky Rats

The aim of the present study was to determine the receptor subtype involved in arginine vasopressin (AVP)-induced modulation of baroreflex function in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats using novel nonpeptide AVP V1- and V2-receptor antagonists. Baroreceptor heart rate (HR) reflex was investigated in both SHR and WKY rats which were intravenously administered the selective V1- and V2-receptor antagonists OPC-21268 and OPC-31260, respectively. Baroreflex function was assessed by obtaining alternate pressor and depressor responses to phenylephrine and sodium nitroprusside, respectively, to construct baroreflex curves. In both SHR and WKY rats baroreflex activity was tested before and after intravenous administration of vehicle (20% DMSO), OPC-21268 (10 mg/kg), and OPC-31260 (1 and 10 mg/kg). Vehicle did not significantly alter basal mean arterial pressure (MAP) and HR values or baroreflex function in SHR or WKY rats. The V1-receptor antagonist had no significant effect on resting MAP or HR values or on baroreflex parameters in both groups of rats, although this dose was shown to significantly inhibit the pressor response to AVP (5 ng iv; ANOVA, P < 0.05). In SHR but not WKY rats the V2-receptor antagonist significantly attenuated the gain (or slope) of the baroreflex curve (to 73 ± 3 and 79 ± 7% of control for 1 and 10 mg/kg, respectively), although AVP-induced pressor responses were also attenuated with the higher dose of the V2-receptor antagonist. These findings suggest that AVP tonically enhances baroreflex function through a V2 receptor in the SHR.

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