Effects of Ketanserin – a Serotonin Receptor Antagonist – on Placental Blood Flow, Placental Weight and Fetal Weight of Spontaneously Hypertensive Rats and Normal Wistar Kyoto Rats

1991 ◽  
Vol 32 (2) ◽  
pp. 65-67 ◽  
Author(s):  
N. Furuhashi ◽  
M. Tsujiei ◽  
H. Kimura ◽  
A. Yajima
Keyword(s):  
Blood Flow ◽  
Receptor Antagonist ◽  
Spontaneously Hypertensive Rats ◽  
Serotonin Receptor ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Placental Blood ◽  
Wistar Kyoto ◽  
Serotonin Receptor Antagonist ◽  
Placental Blood Flow

Excess oxygen delivery during muscle contractions in spontaneously hypertensive rats

1995 ◽  
Vol 78 (1) ◽  
pp. 101-111 ◽  
Author(s):  
J. M. Lash ◽  
H. G. Bohlen
Keyword(s):  
Blood Flow ◽  
Oxygen Saturation ◽  
Oxygen Delivery ◽  
Spontaneously Hypertensive Rats ◽  
Muscle Contractions ◽  
Hypertensive Rats ◽  
Hemoglobin Oxygen Saturation ◽  
Spontaneously Hypertensive ◽  
Tissue Po2 ◽  
Wistar Kyoto

These experiments determined whether a deficit in oxygen supply relative to demand could account for the sustained decrease in tissue PO2 observed during contractions of the spinotrapezius muscle in spontaneously hypertensive rats (SHR). Relative changes in blood flow were determined from measurements of vessel diameter and red blood cell velocity. Venular hemoglobin oxygen saturation measurements were performed by using in vivo spectrophotometric techniques. The relative dilation [times control (xCT)] of arteriolar vessels during contractions was as large or greater in SHR than in normotensive rats (Wistar-Kyoto), as were the increases in blood flow (2 Hz, 3.50 +/- 0.69 vs. 3.00 +/- 1.05 xCT; 4 Hz, 10.20 +/- 3.06 vs. 9.00 +/- 1.48 xCT; 8 Hz, 16.40 +/- 3.95 vs. 10.70 +/- 2.48 xCT). Venular hemoglobin oxygen saturation was lower in the resting muscle of SHR than of Wistar-Kyoto rats (31.0 +/= 3.0 vs. 43.0 +/- 1.9%) but was higher in SHR after 4- and 8-Hz contractions (4 Hz, 52.0 +/- 4.8 vs. 43.0 +/- 3.6%; 8 Hz, 51.0 +/- 4.6 vs. 41.0 +/- 3.6%). Therefore, an excess in oxygen delivery occurs relative to oxygen use during muscle contractions in SHR. The previous and current results can be reconciled by considering the possibility that oxygen exchange is limited in SHR by a decrease in anatomic or perfused capillary density, arteriovenular shunting of blood, or decreased transit time of red blood cells through exchange vessels.

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.

Cerebral artery responses to pressure and flow in uremic hypertensive and spontaneously hypertensive rats

2003 ◽  
Vol 284 (4) ◽  
pp. H1212-H1216 ◽  
Author(s):  
D. I. New ◽  
A. M. S. Chesser ◽  
R. C. Thuraisingham ◽  
M. M. Yaqoob
Keyword(s):  
Blood Flow ◽  
Cerebral Artery ◽  
Spontaneously Hypertensive Rats ◽  
Perfusion Pressure ◽  
Hypertensive Rats ◽  
Independent Manner ◽  
Spontaneously Hypertensive ◽  
Cerebral Blood Flow Autoregulation ◽  
Wistar Kyoto ◽  
Normotensive Control

Impaired cerebral blood flow autoregulation is seen in uremic hypertension, whereas in nonuremic hypertension autoregulation is shifted toward higher perfusion pressure. The cerebral artery constricts in response to a rise in either lumen pressure or flow; we examined these responses in isolated middle cerebral artery segments from uremic Wistar-Kyoto rats (WKYU), normotensive control rats (WKYC), and spontaneously hypertensive rats (SHR). Pressure-induced (myogenic) constriction developed at 100 mmHg; lumen flow was then increased in steps from 0 to 98 μl/min. Some vessels were studied after endothelium ablation. Myogenic constriction was significantly lower in WKYU (28 ± 2.9%) compared with both WKYC (39 ± 2.5%, P = 0.035) and SHR (40 ± 3.1%, P = 0.018). Flow caused constriction of arteries from all groups in an endothelium-independent manner. The response to flow was similar in WKYU and WKYC, whereas SHR displayed increased constriction compared with WKYU ( P < 0.001) and WKYC ( P < 0.001). We conclude that cerebral myogenic constriction is decreased in WKYU, whereas flow-induced constriction is enhanced in SHR.

Resetting of renal blood flow autoregulation in spontaneously hypertensive rats

1987 ◽  
Vol 252 (3) ◽  
pp. F480-F486 ◽  
Author(s):  
B. M. Iversen ◽  
I. Sekse ◽  
J. Ofstad
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Spontaneously Hypertensive Rats ◽  
Lower Pressure ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Pressure Limit ◽  
Wistar Kyoto ◽  
Renal Vascular ◽  
Renal Blood Flow Autoregulation

Renal blood flow (RBF) autoregulation was examined in untreated 10- and 40-wk-old spontaneously hypertensive rats (SHR) [mean arterial pressure (MAP) 125 +/- 4 and 167 +/- 7 mmHg] and in captopril-treated (7 days) 10- and 40-wk-old SHR (88 +/- 7 and 112 +/- 5 mmHg). Age-matched Wistar-Kyoto rats (WKY) were used as controls (MAP 91 +/- 3 and 104 +/- 2 mmHg). The study was carried out in rats with and without acute uninephrectomy. In 10-wk-old acutely uninephrectomized animals, the lower pressure limit of autoregulation was 78 +/- 4 mmHg in WKY, 102 +/- 5 mmHg in SHR (P less than 0.02), and 78 +/- 7 mmHg in captopril-treated SHR (P greater than 0.10). The renal vascular resistance (RVR) was significantly elevated at the lower pressure limit of RBF autoregulation in untreated SHR (P less than 0.02) but became normal after treatment (P greater than 0.10). Neither uninephrectomy nor variation of RBF between different batches seemed to influence the lower pressure limit of RBF autoregulation. In 40-wk-old acutely nephrectomized animals, the lower pressure limit of RBF autoregulation in WKY was 85 +/- 4 mmHg, 128 +/- 3 mmHg in SHR (P less than 0.001), and 101 +/- 5 mmHg in captopril-treated SHR (P less than 0.01). RVR at the lower pressure limit was increased in untreated SHR (P less than 0.01), but fell to normal values during captopril treatment. Neither the uninephrectomy nor variation of RBF between different batches of rats seemed to influence the lower pressure limit of RBF autoregulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Impaired hemodynamics and endothelial vasomotor function via endoperoxide-mediated vasoconstriction in the carotid artery of spontaneously hypertensive rats

2009 ◽  
Vol 296 (4) ◽  
pp. H1038-H1047 ◽  
Author(s):  
Steven G. Denniss ◽  
James W. E. Rush
Keyword(s):  
Blood Flow ◽  
Carotid Artery ◽  
Spontaneously Hypertensive Rats ◽  
Contractile Activity ◽  
Body Wave ◽  
Large Artery ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Vasomotor Function ◽  
Wistar Kyoto

The fact that endothelium removal increases diameter and compliance in the common carotid artery (CCA) of spontaneously hypertensive rats (SHR) and that improving CCA endothelium-dependent vasorelaxation has been shown to normalize a reduced systolic blood flow through the SHR CCA compared with normotensive Wistar-Kyoto rats (WKY) suggests that endothelial vasomotor dysfunction may be linked to altered large artery hemodynamics in hypertension. The experiments herein were designed to further investigate WKY and SHR CCA hemodynamics and endothelium-dependent vasomotor functions. It was hypothesized that CCA blood flow and conductance would be reduced throughout the cardiac cycle in SHR and that endothelium-dependent contractile activity would impair SHR CCA vasorelaxation. We report that mean, maximal systolic, and diastolic blood flow was reduced in SHR vs. WKY CCA, as was vascular conductance. Pressure was augmented in SHR CCA and accompanied by late systolic flow augmentation so that total flow during systole was indeed no different between strains, possibly explained by earlier lower body wave reflection. While ACh stimulation in isolated precontracted WKY CCA caused a robust nitric oxide (NO)-mediated vasorelaxation, endothelium-dependent, cyclooxygenase (COX)-mediated contractile activity stimulated by high ACh concentration impaired NO- and non-NO/non-COX-mediated vasorelaxation in precontracted SHR CCA. In quiescent CCA, this endothelium-dependent contractile response was COX-1 and thromboxane-prostanoid receptor mediated and modulated by the availability of NO. These data collectively suggest that endothelium-dependent, COX-mediated endoperoxide signaling in the CCA of SHR may elicit vasoconstriction, which could shift the mechanical properties of this conduit artery and contribute to reduced CCA blood flow in vivo.

scholarly journals The pancreatic islets in spontaneously hypertensive rats: islet blood flow and insulin production

2001 ◽  
pp. 169-178 ◽  
Author(s):  
M Iwase ◽  
S Sandler ◽  
PO Carlsson ◽  
C Hellerstrom ◽  
L Jansson
Keyword(s):  
Blood Flow ◽  
Spontaneously Hypertensive Rats ◽  
Endocrine Function ◽  
Insulin Biosynthesis ◽  
Insulin Production ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Essentially Normal ◽  
Islet Blood Flow ◽  
Wistar Kyoto

The aim of the study was to investigate if hypertension affects pancreatic islet blood flow and endocrine function. For this purpose, spontaneously hypertensive rats (SHR) were compared with normotensive control Wistar-Kyoto rats (WKY). Both islet size and islet cell replication in 4-month-old SHR was increased compared with WKY. The (pro)insulin biosynthesis was reduced in islets isolated from SHR, whereas the insulin content was unchanged. A hyperinsulinemic response to glucose in vivo was observed in 4- and 12-month-old SHR. Pancreatic blood flow, measured using a microsphere technique, was lower in SHR than in WKY in rats aged 5 weeks, 4 months or 1 year. Islet blood flow was lower in 4-month-old and 1-year-old SHR. In 4-month-old animals, islet blood flow was unaffected by administration of enalaprilate and prazosin in both strains, but was markedly decreased by the administration of N(G)-methyl-L-arginine. It was concluded that the islets of SHR have a decreased insulin production in vitro and a decreased islet blood perfusion. The reasons for this are likely to be multifactorial. Because SHR maintained an essentially normal glucose tolerance, an adaptation of the beta-cells to the metabolic and hemodynamic changes imposed by hypertension occurred.

Arterial and arteriolar contributions to skeletal muscle functional hyperemia in spontaneously hypertensive rats

1995 ◽  
Vol 78 (1) ◽  
pp. 93-100 ◽  
Author(s):  
J. M. Lash
Keyword(s):  
Blood Flow ◽  
Spontaneously Hypertensive Rats ◽  
Muscle Blood Flow ◽  
Muscle Contractions ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Tissue Po2 ◽  
Wistar Kyoto ◽  
Induced Changes

During contractions of the spinotrapezius muscle in spontaneously hypertensive rats (SHR), arteriolar dilation is of normal magnitude but tissue PO2 is significantly depressed relative to normotensive [Wistar-Kyoto (WKY)] rats. This study examined the possibility that this low PO2 results from suppressed dilation of the upstream arterial feed vessels and a limitation of muscle blood flow. Contraction-induced changes in vascular resistances (R) and conductances (G) were calculated for upstream (Rup, Gup), microvascular (Rst, Gst), and downstream (Rdown, Gdown) vascular segments from measurements of pressure and flow in the rostral feed artery and vein. Feed arteries were smaller in SHR than in WKY rats at rest and after contractions (rest, 63.0 +/- 2.6 vs. 86.0 +/- 4.8 microns; 2 Hz 84.0 +/- 4.5 vs. 111.0 +/- 7.3 microns; 8 Hz, 130.0 +/- 5.9 vs. 144.0 +/- 7.1 microns). However, relative increases [times control (xCT)] in diameter and flow were greater in SHR (8 Hz diam, 2.080 +/- 0.072 vs. 1.690 +/- 0.042 xCT; 8 Hz flow, 15.700 +/- 2.057 vs. 8.170 +/- 0.752 xCT). In both groups, Rup and Rst decreased 60–70 and 85–90% after 2- and 8-Hz contractions, respectively. However, segmental vascular conductances increased more in SHR than in WKY rats (8 Hz: Gup, 18.50 +/- 3.76 vs. 8.00 +/- 1.26 xCT; Gst, 19.90 +/- 3.73 vs. 10.10 +/- 0.96 xCT; Gdown, 8.80 +/- 1.70 vs. 5.50 +/- 0.88 xCT). Therefore, upstream arterial dilation is not suppressed during muscle contractions in SHR, and deficits in muscle blood flow and oxygen delivery cannot account for the abnormally low tissue PO2 observed during muscle contractions in SHR.

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