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 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.

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 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.

scholarly journals Sustained density of neuroendocrine cells with aging precedes development of prostatic hyperplasia in spontaneously hypertensive rats

BMC Urology ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Yuki Kyoda ◽  
Koji Ichihara ◽  
Kohei Hashimoto ◽  
Ko Kobayashi ◽  
Fumimasa Fukuta ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Prostatic Hyperplasia ◽  
Neuroendocrine Cells ◽  
Initial Growth ◽  
Hypertensive Rats ◽  
Initial Development ◽  
Spontaneously Hypertensive ◽  
Significant Difference ◽  
The Difference ◽  
Wistar Kyoto

Abstract Background Neuroendocrine (NE) cells may have an impact on the development and initial growth of benign prostatic hyperplasia (BPH) according to previous human studies. Methods To explore the relationship of NE cells and BPH development, we compared the density of NE cells and also prostatic weight in spontaneously hypertensive rats (SHR), which develop by aging, and Wistar-Kyoto rats (WKY) as control. The total weights of the epithelium and stroma in the ventral lobes of 8-, 12, 16-, 28- and 56-week-old SHR and WKY were calculated using Image J software. NE cells in the ventral prostatic ducts (VPd) were quantified using immunohistochemical staining for serotonin. Results Although there was no significant difference in the estimated total weight of the epithelium and stroma in the ventral lobes adjusted by body weight (ES weight) between the two groups at 8, 12 and 16 weeks of age, ES weight was significantly greater in the SHR group than in the WKT group at 28 and 56 weeks. The density of NE cells in the VPd decreased with aging in the WKY group, whereas it was sustained until 16 weeks and then decreased with aging in the SHR group. The difference in the density between the two groups was most marked at 16 weeks of age. Conclusion In the natural history of BPH, NE cells may play an important role in the initial development of BPH because sustained density of NE cells in the VPd precedes the development of prostatic hyperplasia.

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.

α2-Adrenergic receptors in NTS facilitate baroreflex function in adult spontaneously hypertensive rats

2002 ◽  
Vol 282 (6) ◽  
pp. H2336-H2345 ◽  
Author(s):  
Linda F. Hayward ◽  
Alecia P. Riley ◽  
Robert B. Felder
Keyword(s):  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Spontaneously Hypertensive ◽  
Aortic Depressor Nerve ◽  
Baroreflex Function ◽  
Wistar Kyoto ◽  
Renal Sympathetic

We examined the effect of α2-adrenoreceptor blockade in the nucleus of the solitary tract (NTS) on baroreflex responses elicited by electrical stimulation of the left aortic depressor nerve (ADN) in urethane-anesthetized spontaneously hypertensive rats (SHR, n = 11) and normotensive Wistar-Kyoto rats (WKY, n = 11). ADN stimulation produced a frequency-dependent decrease in mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), and heart rate (HR). In SHR, unilateral microinjection of idazoxan into the NTS markedly reduced baroreflex control of MAP, RSNA, and HR and had a disproportionately greater influence on baroreflex control of MAP than of RSNA. In WKY, idazoxan microinjections did not significantly alter baroreflex function relative to control vehicle injections. These results suggest that baroreflex regulation of arterial pressure in SHR is highly dependent on NTS adrenergic mechanisms. The reflex regulation of sympathetic outflow to the kidney is less influenced by the altered α2-adrenoreceptor mechanisms in SHR.

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.

Role of thromboxane in control of arterial pressure and renal function in young spontaneously hypertensive rats

1986 ◽  
Vol 250 (3) ◽  
pp. F488-F496 ◽  
Author(s):  
H. J. Grone ◽  
R. S. Grippo ◽  
W. J. Arendshorst ◽  
M. J. Dunn
Keyword(s):  
Renal Function ◽  
Arterial Pressure ◽  
Receptor Antagonist ◽  
Spontaneously Hypertensive Rats ◽  
Renal Plasma Flow ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Txa2 Receptor ◽  
Wistar Kyoto ◽  
Txa2 Receptor Antagonist

As platelet and renal thromboxane (TX)A2 synthesis are increased in spontaneously hypertensive rats (SHR), we tested the hypothesis that increased renal TXA2 synthesis may cause the reduction in glomerular filtration rate (GFR), renal plasma flow (RPF), and the increase in arterial pressure in SHR of the Okamoto-Aoki strain. A selective inhibitor of TXA2 synthetase (UK 38485) was given acutely, with or without a TXA2 receptor antagonist (EP-092), to 6- to 8-wk-old SHR and age-matched Wistar-Kyoto rats (WKY) and chronically for 5.5 wk to 3.5-wk-old SHR. Inhibition of TXA2, measured by the stable metabolite TXB2, in the acute experiments was greater than 95% in serum and greater than 80% in glomeruli; in the chronic studies, it was greater than 65% in glomeruli. There was no endoperoxide shunting to vasodilatory and natriuretic prostaglandins (PGE2, PGI2) in glomeruli after TXA2 inhibition. Before drug administration, GFR and RPF were reduced and renal vascular resistance (RVR) was increased in SHR. During acute blockade of renal TXA2 synthesis, with or without a TXA2 receptor antagonist, there was no significant change in GFR, RPF, or RVR in WKY and SHR. Inhibition of TXA2 did not affect urine flow or sodium excretion in anesthetized or conscious WKY or SHR. Mean arterial pressure did not fall in treated SHR and WKY. Chronic TXA2 synthesis inhibition did not improve GFR or RPF in SHR, and systolic arterial pressure was not altered. These findings show that enhanced serum and glomerular TXA2 synthesis do not significantly contribute to the reduction in renal function and are not essential for the development of hypertension in young SHR.

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.

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