Microvascular adaptation in the cerebral cortex of adult spontaneously hypertensive rats.

Abstract

The purpose of this study was to determine the microvascular characteristics that cause cerebral cortical blood flow autoregulation to shift to a higher range of arterial pressures during established hypertension in spontaneously hypertensive rats (SHR). An open-skull technique with constant suffusion of artificial cerebrospinal fluid (PO2 = 40-45 mm Hg, PCO2 = 40-45 mm Hg, pH = 7.35-7.45) was used to view the parietal cortex of 18- to 21-week-old SHR and Wistar Kyoto (WKY) normotensive control rats. The resting inner diameters of first (1A)-, second (2A)-, and fourth (4a)-order arterioles were significantly (p less than 0.05) smaller, and the wall thickness/lumen diameter ratios were significantly (p less than 0.05) larger in SHR compared to WKY. Only 1A and 4A has significantly (p less than 0.05) increased vessel wall cross-sectional area in SHR. At the resting mean arterial pressures of WKY and SHR, the passive (10(-4) M adenosine, topical) diameters of comparable types of arterioles were not significantly different (p greater than 0.05). At reduced arterial pressures, however, the arterioles in SHR had smaller maximum diameters than in WKY. Cortical blood flow in WKY and SHR was constant at arterial pressures from 70-150 mm Hg and 100-200 mm Hg, respectively. Resting arteriolar pressures in 1A, 2A, and 3A of SHR were substantially and significantly (p less than 0.05) elevated, although pressures in the smallest arterioles and venules of WKY and SHR were similar. Therefore, it is possible that cerebral capillary pressure is only slightly elevated, if at all, in SHR as a result of the vasoconstriction. The number of arterioles per unit area of brain surface at rest was equal in WKY and SHR. In addition, the number of vessels was equal in WKY and SHR during maximal dilation, and neither type of rat demonstrated an opening of previously closed vessels upon maximum dilation. Therefore, the cerebral arteriolar constriction in SHR, which was probably potentiated by vessel wall hypertrophy of the largest and smallest arterioles, was the major contributor to an upward shift in the autoregulatory range, the protection of exchange vasculature pressures, and the increase in vascular resistance.

Circulating IGF-1 deficiency exacerbates hypertension-induced microvascular rarefaction in the mouse hippocampus and retrosplenial cortex: implications for cerebromicrovascular and brain aging

“…8c). There is strong evidence that in healthy young animals pressure-induced myogenic constriction of proximal arterial branches of the cerebrovascular tree acts as a critical homeostatic mechanism that assures that increased systemic arterial pressure cannot penetrate the distal portion of the cerebral microcirculation and cause damage to the thin-walled arteriolar and capillary microvessels (Toth et al 2013a;Toth et al 2014a;Kontos et al 1978;Harper and Bohlen 1984). In cerebral resistance arteries isolated from hypertensive young control animals (Toth et al 2013a;Toth et al 2013b), the myogenic constriction at high pressures is augmented, suggesting that the pressure range for autoregulatory cerebrovascular protection is extended.…”

Enhanced Parenchymal Arteriole Tone and Astrocyte Signaling Protect Neurovascular Coupling Mediated Parenchymal Arteriole Vasodilation in the Spontaneously Hypertensive Rat

“…As a general rule, larger diameter PAs require higher flow rates to develop myogenic tone whereas smaller diameter PAs need minimal flow to develop myogenic tone. Further, high flow rates are needed to attain luminal pressures in the physiologic range (27 to 34 mm Hg 47 ) resulting in high SS. Because lower flow rates are favored to maintain low SS values, the PA pressures reported in our study are below previously reported in vivo pressures for arterioles of similar magnitude.…”

Remodeling of cerebral arterioles in chronic hypertension.

“…8 There may be two reasons for the apparent discrepancy in findings. First, internal diameter of passive pial arterioles was measured at prevailing levels of systemic arterial pressure in both normotensive and hypertensive rats.…”

“…First, internal diameter of passive pial arterioles was measured at prevailing levels of systemic arterial pressure in both normotensive and hypertensive rats. 8 In contrast, we measured internal diameter of passive arterioles at the same level of pial arteriolar pressure (70 mm Hg) in the two groups of rats. Second, rats were examined at a younger age (18-21 weeks old) in the previous study 8 than in this study (10-12 months old).…”

“…8 In contrast, we measured internal diameter of passive arterioles at the same level of pial arteriolar pressure (70 mm Hg) in the two groups of rats. Second, rats were examined at a younger age (18-21 weeks old) in the previous study 8 than in this study (10-12 months old). We have shown previously 6 that internal diameter of pial arterioles during maximal dilatation is significantly less in SHRSP than in WKY rats at 6-8 months of age, but not at 3 months of age.…”