Plasma parathyroid hormone during the development of spontaneous hypertension in rats

1987 ◽  
Vol 65 (12) ◽  
pp. 2386-2389 ◽  
Author(s):  
P. K. T. Pang ◽  
S. Harvey ◽  
P. A. Doris
Keyword(s):  
Parathyroid Hormone ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneous Hypertension ◽  
Hypertensive Rats ◽  
Intact Pth ◽  
Spontaneously Hypertensive ◽  
Blood Pressures ◽  
Wistar Kyoto ◽  
Tail Cuff

Plasma parathyroid hormone levels (pPTH) have been measured by radioimmunoassay (RIA) in young spontaneously hypertensive rats (SHR) and normotensive Wistar–Kyoto controls (WKY) aged from 6 to 16 weeks to assess the possible role of PTH during the development of hypertension. Three antisera were used in the RIAs. One antiserum was directed toward the inactive C-terminal fragment of PTH, another toward the bioactive N-terrninal fragment (PTH 1–34), and a third was obtained by immunization against intact PTH 1–84. Blood pressures were measured by tail-cuff plethysmography with prewarming. Blood ionized calcium and sodium concentrations (b[Ca2+] and b[Na+]) were determined by ion-selective electrolyte analysis. No significant differences were observed between pPTH in the SHR compared with WKY during the development of hypertension. Neither were significant differences in b[Ca2+] or b[Na+] present at any age. The expected progression of hypertension in SHRs was observed and blood pressure was significantly greater in SHR than in WKY at all times. The results suggest that differences in pPTH and b[Ca2+] in SHR reported in other studies may be secondary phenomena to the establishment of hypertension. Our data suggest that PTH is not involved in the pathogenetic processes occurring during the development of spontaneous hypertension in rats.

Norepinephrine levels in paraventricular nucleus of spontaneously hypertensive rats: role of neuropeptide Y

1993 ◽  
Vol 265 (3) ◽  
pp. H893-H898 ◽  
Author(s):  
N. D. Woo ◽  
K. Mukherjee ◽  
P. K. Ganguly
Keyword(s):  
Neuropeptide Y ◽  
Paraventricular Nucleus ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Central Neurons ◽  
Sympathetic Regulation ◽  
Series Of Experiments ◽  
Wistar Kyoto

Recent evidence supports the view that the sympathetic system actively participates in the development of hypertension. Because norepinephrine, contained within central neurons involved in cardiovascular sympathetic regulation, is known to coexist with neuropeptide Y, it is possible that a functional interaction between neuropeptide Y and norepinephrine exists within the brain. In an effort to clarify whether or not central catecholamine systems are modulated by neuropeptide Y in hypertensive situations, the paraventricular nucleus of spontaneously hypertensive rats was exposed to neuropeptide Y (10(-9) M), and levels of norepinephrine were sampled by microdialysis. Norepinephrine levels in spontaneously hypertensive rats were significantly increased and did not change after exposure to neuropeptide Y, in sharp contrast to the decreases seen in Wistar-Kyoto controls. To ascertain whether these alterations in norepinephrine control were specific to the model used, a similar series of experiments was carried out in the paraventricular nucleus of aortic-banded rats. These studies supported the previous findings. Norepinephrine levels in aortic-banded rats were markedly elevated when compared with sham-operated controls and demonstrated no change after exposure to neuropeptide Y, whereas decreases of > 50% were seen in sham-operated controls. These results support the view that mechanisms normally involving neuropeptide Y as a neuromodulator in the paraventricular nucleus are altered in hypertensive situations. It is suggested that hypertension may precipitate changes in mechanisms involving brain neuropeptide Y and increased sympathetic activity.

scholarly journals Role of cholinergic receptors in adrenal catecholamine secretion in spontaneously hypertensive rats

1999 ◽  
Vol 277 (4) ◽  
pp. R1057-R1062 ◽  
Author(s):  
Takahiro Nagayama ◽  
Takayuki Matsumoto ◽  
Makoto Yoshida ◽  
Mizue Suzuki-Kusaba ◽  
Hiroaki Hisa ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Muscarinic Receptors ◽  
Nicotinic Receptors ◽  
Spontaneously Hypertensive Rats ◽  
Adrenal Glands ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto

We investigated the role of nicotinic and muscarinic receptors in secretion of catecholamines induced by transmural electrical stimulation (ES) from isolated perfused adrenal glands of spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats. ES (1–10 Hz) produced frequency-dependent increases in epinephrine (Epi) and norepinephrine (NE) output as measured in perfusate. The ES-induced increases in NE output, but not Epi output, were significantly greater in adrenal glands of SHRs than in those of WKY rats. Hexamethonium (10–100 μM) markedly inhibited the ES-induced increases in Epi and NE output from adrenal glands of SHRs and WKY rats. Atropine (0.3–3 μM) inhibited the ES-induced increases in Epi and NE output from adrenal glands of SHRs, but not from those of WKY rats. These results suggest that endogenous acetylcholine-induced secretion of adrenal catecholamines is predominantly mediated by nicotinic receptors in SHRs and WKY rats and that the contribution of muscarinic receptors may be different between these two strains.

scholarly journals Role of NO on pressure-natriuresis in Wistar-Kyoto and spontaneously hypertensive rats

1993 ◽  
Vol 43 (1) ◽  
pp. 205-211 ◽  
Author(s):  
Hideki Ikenaga ◽  
Hiromichi Suzuki ◽  
Naohito Ishii ◽  
Hajime Itoh ◽  
Takao Saruta
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Pressure Natriuresis

Calcium reactivity and antagonism in portal veins from spontaneously hypertensive and normotensive rats

1984 ◽  
Vol 62 (1) ◽  
pp. 146-150 ◽  
Author(s):  
A. L. Harris ◽  
V. C. Swamy ◽  
D. J. Triggle
Keyword(s):  
Inhibitory Activity ◽  
Spontaneously Hypertensive Rats ◽  
Age Groups ◽  
Induced Responses ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Activity Frequency ◽  
Blood Pressures ◽  
Portal Veins ◽  
Wistar Kyoto

Reactivities of portal veins from spontaneously hypertensive rats (SHR) and normotensive controls (Wistar Kyoto, WKY) at 5–7 and 15–17 weeks of age were compared. Systolic blood pressures were not different at 5–7 weeks but those of SHR were significantly elevated (177 ± 4 mmHg) (1 mmHg = 133.322 Pa) at 15–17 weeks. Spontaneous activity, frequency, and tension were greater in SHR for both age groups. Young SHR were more sensitive to K+ at 5–7 weeks but less sensitive at 15–17 weeks than age-matched WKY rats. Sensitivity to Ca2+ in a K+-depolarizing medium was higher in SHR than in WKY for both age groups. Maximum tension responses to K+ or Ca2+ were greater in SHR. The Ca2+ channel antagonists nifedipine, nitrendipine, and nisoldipine were potent inhibitors of both noradrenaline- and K+-induced responses but did not show differences in inhibitory activity between WKY and SHR.

Diminished sympathetic silent period in spontaneously hypertensive rats

1979 ◽  
Vol 236 (3) ◽  
pp. R147-R152 ◽  
Author(s):  
L. P. Schramm ◽  
G. N. Barton
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Activity ◽  
Spontaneously Hypertensive Rats ◽  
Silent Period ◽  
Spontaneous Hypertension ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Splanchnic Nerves ◽  
Wistar Kyoto ◽  
Stimulation Of

To determine if elevated sympathetic activity occurs in spontaneously hypertension, the silent period induced in splanchnic nerves following electrical stimulation of dorsal medullary sympathoexcitatory sites was compared in anesthetized normotensive Wistar Kyoto rats (WKYs) and Okamoto spontaneously hypertensive rats (SHRs). The strength of silent periods was defined as the degree of inhibition of responses to testing stimuli delivered at various latencies following conditioning trains, and it was assumed to be inversely related to the level of sympathetic activity. Weanling SHRs exhibited weaker silent periods than weanling WKYs although, at that age, the arterial pressures of the strains were not significantly different. Silent periods were also weaker in adult SHRs than in adult WKYs. This difference persisted after arterial pressures, which fell under anesthesia, were raised by phenylephrine infusions to the respective "normal" levels in each strain. These results support the hypothesis that elevated sympathetic activity exists during both the development and maintenance of spontaneous hypertension in rats.

Role of endogenous centrally released NO in cardiovascular adaptation to hypovolemia in WKY and SHR

1997 ◽  
Vol 272 (5) ◽  
pp. H2282-H2288 ◽  
Author(s):  
P. Paczwa ◽  
A. S. Budzikowski ◽  
E. Szczepanska-Sadowska
Keyword(s):  
Heart Rate ◽  
Spontaneously Hypertensive Rats ◽  
Hypotensive Effect ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Time Control ◽  
Artificial Cerebrospinal Fluid ◽  
In Series ◽  
Wistar Kyoto

The role of endogenous centrally released nitric oxide (NO) during hypovolemia was investigated in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Bleeding of the rats (1.3% of blood volume) was performed after intracerebroventricular (ICV) administration of: 1) artificial cerebrospinal fluid (series 1, time control, 8 WKY and 8 SHR); 2) 0.5 mg NG-nitro-L-arginine (L-NNA, 2.3 nmol), an inhibitor of NO synthesis (series 2, 8 WKY and 7 SHR); and 3) 0.5 mg L-NNA followed by 1 mg (5.8 nmol) of L-arginine (L-Arg) (6 WKY and 5 SHR). In WKY, hypotension was associated with significant bradycardia (P < 0.001), whereas in SHR slight acceleration of heart rate was observed. In series 2 hemorrhage resulted in a small but significant increase of mean arterial pressure (MAP; P < 0.05) and considerable tachycardia (P < 0.001). In SHR, L-NNA did not modify the decrease of MAP during hypovolomia, and bleeding resulted in a significant bradycardia (P < 0.001). Pretreatment with L-Arg in series 3 was able to reverse the effects of L-NNA on changes of MAP and heart rate during hypovolemia. The results indicate that the central nitroxidergic system plays a significant role in eliciting hypotension and bradycardia in normotensive WKY during hemorrhage. Function of the central nitroxidergic system is significantly altered in SHR in which NO appears to prevent hemorrhagic bradycardia and to reduce the hypotensive effect.

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.

Chronic exercise decreases adrenergic agonist-induced vasoconstriction in spontaneously hypertensive rats

1996 ◽  
Vol 271 (3) ◽  
pp. H977-H983 ◽  
Author(s):  
H. I. Chen ◽  
I. P. Chiang
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Carotid Arteries ◽  
Peak Oxygen Consumption ◽  
Chronic Exercise ◽  
Hypertensive Rats ◽  
Adrenergic Agonist ◽  
Spontaneously Hypertensive ◽  
Effective Training ◽  
Wistar Kyoto

This study was conducted to investigate the effects of chronic exercise on adrenergic agonist-induced vascular responses in spontaneously hypertensive rats (SHR). Four-week-old male SHR and Wistar-Kyoto rats were divided into control and trained groups. The trained groups ran on a drum exerciser at 70% of peak oxygen consumption for 60 min/day 5 days/wk for 10 wk. Resting systolic blood pressure and heart rate were measured by a tail-cuff method, and changes in these parameters were considered as indexes of effective training. At the end of experiments, thoracic aortas and carotid arteries were isolated. Vasoconstricting responses to norepinephrine (NE) or phenylephrine (PHE) were studied. To clarify the role of endothelium-derived nitric oxide (EDNO) in the alteration of NE-induced vasoconstriction after chronic exercise, we measured the changes in vasoconstricting responses to NE (10(-8) M) after treatment with N omega-nitro-L-arginine. Vasorelaxing responses to PHE or clonidine were also studied. Our results showed that 1) vasoconstricting responses to NE or PHE in the endothelium-intact thoracic aorta were reduced, whereas PHE- or clonidine-induced EDNO release was enhanced by exercise training, and 2) the latter could be eliminated by N omega-nitro-L-arginine. Therefore, training may decrease adrenergic agent-induced vasoconstricting responses by increasing their stimulated EDNO release in hypertensive and normotensive rats.

scholarly journals Effects of hypertension on maternal adaptations to pregnancy: experimental study on spontaneously hypertensive rats

2001 ◽  
Vol 119 (2) ◽  
pp. 54-58 ◽  
Author(s):  
José Carlos Peraçoli ◽  
Marilza Vieira Cunha Rudge ◽  
Maria Salete Sartori ◽  
Roberto Jorge da Silva Franco
Keyword(s):  
Blood Pressure ◽  
Weight Gain ◽  
Spontaneously Hypertensive Rats ◽  
Sodium Retention ◽  
Shr Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto ◽  
Tail Cuff

CONTEXT: Animal models for essential hypertension have been used for understanding the human pathological conditions observed in pregnant hypertensive women. OBJECTIVE: To study the possible effects of pregnancy on hypertension and of hypertension on pregnancy in spontaneously hypertensive rats (SHR), and in their normotensive Wistar-Kyoto (WKY) counterparts. TYPE OF STUDY: Comparative study using laboratory animals. SETTING: Animal Research Laboratory of Clinical Medicine at the Medical School of Botucatu, São Paulo State University, Brazil. SAMPLE: Ten to twelve-week-old virgin female normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The animals were separated into four groups: 15 pregnant spontaneously hypertensive rats (SHR-P), 10 non-pregnant spontaneously hypertensive rats (SHR-NP), 15 pregnant normotensive rats (WKY-P), and 10 non-pregnant normotensive rats (WKY-NP). MAIN MEASUREMENTS: The blood pressure was evaluated by the tail cuff method, in rats either with or without prior training for the handling necessary for tail cuff measurements. The maternal volemia expansion was indirectly evaluated by weight gain, and by systemic parameters as hematocrit, hemoglobin, total protein, albumin and sodium retention. The perinatal outcome of pregnancy was evaluated by analysis of resorptions, litter size, rate of low weight and number of stillbirths. RESULTS: The late fall in blood pressure in the pregnant SHR strain and in the normotensive WKY strain can only be detected in rats previously trained to accept the handling necessary for the tail cuff measurement. During pregnancy the body weight gain was significantly higher in WKY than in SHR rats. Systemic parameters were significantly lower in pregnant WKY rats than in non-pregnant WKY rats, while no differences were observed between pregnant and non-pregnant SHR groups. In pregnant WKY rats the sodium retention was higher from the 13th day onwards, while in SHR rats this occurred only on the 21st day. The characteristics of reproductive function such as number and weight of fetus, perinatal mortality and the resorption rate were significantly affected in the SHR strain. CONCLUSION: The SHR strain may be considered as a model for chronic hypovolemic maternal hypertension, with the fetal growth retardation being determined by this hypovolemic state.

Sign in / Sign up

Export Citation Format

Share Document