Cerebral vascular changes associated with hemorrhagic stroke in hypertension

1992 ◽  
Vol 70 (4) ◽  
pp. 552-564 ◽  
Author(s):  
John S. Smeda
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Stroke ◽  
Cerebral Arteries ◽  
Cerebral Vasculature ◽  
Vascular Changes ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Upper Limit ◽  
Middle Cerebral Arteries ◽  
Wistar Kyoto

There are a number of alterations that protect the cerebrovasculature from hemorrhagic stroke development during hypertension. The upper limit of cerebral blood flow autoregulation is shifted to higher blood pressure levels; this allows a constant blood flow to be maintained during hypertension. Studies we have performed have indicated that the middle cerebral arteries (MCA) of Wistar–Kyoto stroke-prone spontaneously hypertensive rats (spSHR) lose their ability to constrict in response to elevations in transmural pressure. The decline in such function precedes stroke development and totally disappears at an age where there is a 100% mortality from stroke. Prior to stroke development, spSHR also develop uremic conditions and signs of renal failure. The induction of uremia in stroke-resistant SHR (srSHR) via nephrectomy induces these animals to develop stroke. Like prestroke spSHR, prestroke uremic srSHR also have MCA with attenuated pressure-dependent myogenic function. It is hypothesized that the inability to increase vascular resistance in response to elevations in pressure might promote overperfusion of the more distal vasculature leading to cerebral hemorrhage formation. Since uremia promotes bleeding tendencies, such alterations along with the loss of cerebrovascular myogenic function could initiate or aggrevate hemorrhage formation.Key words: stroke-prone SHR, stroke, cerebral vasculature, myogenic response, autoregulation.

Sex-specific differences in cerebral arterial myogenic tone in hypertensive and normotensive rats

2006 ◽  
Vol 290 (3) ◽  
pp. H1081-H1089 ◽  
Author(s):  
Jamila Ibrahim ◽  
Ann McGee ◽  
Delyth Graham ◽  
John C. McGrath ◽  
Anna F. Dominiczak
Keyword(s):  
Blood Flow ◽  
Cerebral Arteries ◽  
Systemic Blood Pressure ◽  
Limiting Factors ◽  
Myogenic Tone ◽  
Spontaneously Hypertensive ◽  
Cerebrovascular Events ◽  
Middle Cerebral Arteries ◽  
Wistar Kyoto ◽  
Strain Dependent

Cerebral blood flow (CBF) is maintained constant despite changes in systemic blood pressure (BP) through multiple mechanisms of autoregulation such as vascular myogenic reactivity. Our aim was to determine myogenic characteristics of cannulated middle cerebral arteries (MCA) in male and female stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto rats (WKY) at 12 wk of age under pressurised no-flow conditions. MCA pressure-diameter relationships (20–200 mmHg) were constructed in active (with calcium) and passive (without calcium) conditions, and myogenic and mechanical properties were determined. Myogenic reactivity in WKY ( P < 0.05) and SHRSP ( P < 0.05) males was impaired compared with their female counterparts. Comparison of SHRSP with WKY in males revealed similar myogenic reactivity, but in females SHRSP exhibited augmented myogenic reactivity ( P < 0.05). In both sexes, myogenic tone yielded at lower pressure in SHRSP compared with WKY vessels (120–140 vs. 140–180 mmHg). Stress-strain relationships and elastic moduli in WKY rats showed that vessels were stiffer in females than in males. Conversely, in SHRSP, male vessels were stiffer than female vessels. Comparison of strains in males indicated that stiffness was increased in SHRSP compared with WKY vessels, whereas the converse was observed in females. These findings demonstrate that MCA myogenic and distensibility characteristics exhibit significant sex- and strain-dependent differences. Inappropriate myogenic adaptation and augmented vascular stiffness, particularly in male SHRSP, are potential limiting factors in blood flow autoregulation and may increase the predisposition for stroke-related cerebrovascular events.

scholarly journals Loss of cerebrovascular Shaker-type K+ channels: a shared vasodilator defect of genetic and renal hypertensive rats

2009 ◽  
Vol 297 (1) ◽  
pp. H293-H303 ◽  
Author(s):  
Ann A. Tobin ◽  
Biny K. Joseph ◽  
Hamood N. Al-Kindi ◽  
Sulayma Albarwani ◽  
Jane A. Madden ◽  
...  
Keyword(s):  
Cerebral Arteries ◽  
Chronic Hypertension ◽  
Mrna Levels ◽  
Hypertensive Rats ◽  
Western Blots ◽  
Spontaneously Hypertensive ◽  
Rat Models ◽  
Middle Cerebral Arteries ◽  
Wistar Kyoto ◽  
Renal Hypertensive Rats

The cerebral arteries of hypertensive rats are depolarized and highly myogenic, suggesting a loss of K+ channels in the vascular smooth muscle cells (VSMCs). The present study evaluated whether the dilator function of the prominent Shaker-type voltage-gated K+ (KV1) channels is attenuated in middle cerebral arteries from two rat models of hypertension. Block of KV1 channels by correolide (1 μmol/l) or psora-4 (100 nmol/l) reduced the resting diameter of pressurized (80 mmHg) cerebral arteries from normotensive rats by an average of 28 ± 3% or 26 ± 3%, respectively. In contrast, arteries from spontaneously hypertensive rats (SHR) and aortic-banded (Ao-B) rats with chronic hypertension showed enhanced Ca2+-dependent tone and failed to significantly constrict to correolide or psora-4, implying a loss of KV1 channel-mediated vasodilation. Patch-clamp studies in the VSMCs of SHR confirmed that the peak K+ current density attributed to KV1 channels averaged only 5.47 ± 1.03 pA/pF, compared with 9.58 ± 0.82 pA/pF in VSMCs of control Wistar-Kyoto rats. Subsequently, Western blots revealed a 49 ± 7% to 66 ± 7% loss of the pore-forming α1.2- and α1.5-subunits that compose KV1 channels in cerebral arteries of SHR and Ao-B rats compared with control animals. In each case, the deficiency of KV1 channels was associated with reduced mRNA levels encoding either or both α-subunits. Collectively, these findings demonstrate that a deficit of α1.2- and α1.5-subunits results in a reduced contribution of KV1 channels to the resting diameters of cerebral arteries from two rat models of hypertension that originate from different etiologies.

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.

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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