Arteriolar closure mediated by hyperresponsiveness to norepinephrine in hypertensive rats

1979 ◽  
Vol 236 (1) ◽  
pp. H157-H164 ◽  
Author(s):  
H. G. Bohlen

This study was designed to determine if a mechanism exists to cause abnormally large number of arterioles to be closed to blood flow in spontaneously hypertensive rats (SHR). The contributions to vessel closure by neural control and constrictor response to norepinephrine were investigated. Normal rats (WKY) and SHR were studied at age 18--20 wk. Their respective mean arterial blood pressures were 100 +/- 4 (SE) and 154 +/- 7 mmHg when anesthetized with 10% urethan and 2% alpha-chloralose (0.6 mg/100 g ip). The number of arterioles open to blood flow was counted in a large portion of the cremasteric muscle before and after denervation. The percent change in control diameter of denervated arterioles was measured during iontophoretic application (2 min) of norepinephrine at dose currents of 10--300 nA. Following denervation, a 22.2 +/- 6.3% (SE) and 61.8 +/- 12 increase in the number of third-order arterioles open to flow occurred in WKY and SHR. The diameters, wall thicknesses, and cross-sectional areas of vessel walls were not significantly (P less than 0.05) different for comparable types of denervated arterioles in WKY and SHR. The percent changes in diameters of arterioles in SHR were 3--5 times greater at all dose currents than for vessels of WKY. These data indicate arteriolar closure occurs with higher incidence in SHR than WKY and is mediated by hyperresponsiveness of arterioles to norepinephrine.

1987 ◽  
Vol 253 (4) ◽  
pp. H933-H940 ◽  
Author(s):  
H. Hashimoto ◽  
R. L. Prewitt ◽  
C. W. Efaw

The microcirculation was studied in the cremaster muscle of one-kidney, one-clip (1K-1C) hypertensive rats and uninephrectomized controls under chloralose-urethan anesthesia 1-2, 4-5, or 8-9 wk following renal artery stenosis. With the use of television microscopy, inside and outside diameters of first (1A) through fourth-order (4A) arterioles were measured before and after vasodilation with 10(-4) M adenosine. Mean arterial blood pressure was significantly elevated in the 1K-1C rats, rising to 170 +/- 6 mmHg by 8-9 wks vs. 93 +/- 2 mmHg in controls. Enhanced vasoconstriction, resulting in closure of arterioles, appeared only in the smaller arterioles of 1K-1C and diminished throughout the development of hypertension. Structural rarefaction appeared later and increased with the development of hypertension. Vasodilated inside diameters of control, but not 1K-1C, 1A, 2A, and 3As, increased with increasing age, leaving the hypertensive arterioles with structurally reduced lumens and increased wall-to-lumen ratios, but without increases in wall cross-sectional areas. Structural lumen reduction appeared first in the 1A and advanced downstream as hypertension developed. Thus vasoconstriction of the smallest arterioles is important initially in renal hypertension, but structural alterations become more important later.


2021 ◽  
Vol 12 ◽  
Author(s):  
Dominga Lapi ◽  
Martina Di Maro ◽  
Nicola Serao ◽  
Martina Chiurazzi ◽  
Maurizio Varanini ◽  
...  

BackgroundSeveral studies indicate that hypertension causes major changes in the structure of the vessel wall by affecting the regulation of blood supply to the tissues. Recently, it has been observed that capillary blood flow is also considerably influenced by the structural arrangement of the microvascular networks that undergo rarefaction (reduction of the perfused vessel number). Therefore, this study aimed to assess the geometric arrangements of the pial arteriolar networks and the arteriolar rhythmic diameter changes in spontaneously hypertensive rats (SHRs).MethodsFluorescence microscopy was utilized to observe in vivo the pial microcirculation through a closed cranial window. Pial arterioles were classified according to Strahler’s method. The arteriolar rhythmic diameter changes were evaluated by a generalization short-time Fourier transform.ResultYoung SHRs showed four orders of vessels while the adult ones only three orders. The diameter, length, and branching number obeyed Horton’s law; therefore, the vessels were distributed in a fractal manner. Larger arterioles showed more asymmetrical branches than did the smaller ones in young SHRs, while in adult SHRs smaller vessels presented asymmetrical branchings. In adult SHRs, there was a significant reduction in the cross-sectional area compared with the young SHRs: this implies an increase in peripheral resistance. Young and adult age-matched normotensive rats did not show significant alterations in the geometric arteriolar arrangement with advancing age, both had four orders of arteriolar vessels, and the peripheral resistance did not change significantly. Conversely, the frequency components evaluated in arteriolar rhythmic diameter changes of young and adult SHRs showed significant differences because of a reduction in the frequency components related to endothelial activity detected in adult SHRs.ConclusionIn conclusion, hypertension progressively causes changes in the microarchitecture of the arteriolar networks with a smaller number of vessels and consequent reduced conductivity, characteristic of rarefaction. This was accompanied by a reduction in the formation and release of independent and dependent – endothelial nitric oxide components regulating arterial vasomotion.


1995 ◽  
Vol 268 (4) ◽  
pp. H1499-H1509 ◽  
Author(s):  
T. L. Yang ◽  
C. Y. Chai ◽  
C. T. Yen

The distribution and reactivity of vasomotor sites in the ventrolateral (VLM) and dorsomedial medulla (DMM) of stroke-prone spontaneously hypertensive rats (SHRSP), spontaneously hypertensive rats (SHR), and Wistar-Kyoto rats (WKY) were compared. Rats were anesthetized with alpha-chloralose and urethan. Baroreceptor denervation and vagotomy were performed. L-Glutamate (Glu, 10 mM, 30 nl) was microinjected into the DMM or VLM to identify vasoactive sites. The extent and the patterns of distribution of these sites in the three strains of rats were similar. The dose-response curve of the vasoactive site was studied with 1–500 pmol of Glu. The maximum responses of blood pressure and renal sympathetic activity were larger and threshold doses of Glu were lower in hypertensive rats. The significance of the differences among the strains was analyzed before and after adjustment for baseline pressure or activity. Most of the differences were statistically significant before baseline adjustment. After baseline adjustment, many differences between the SHRSP and the WKY remained significant. However, the only significant difference detected between the SHR and the WKY was the threshold dose for eliciting renal sympathetic change in the caudal VLM. These results suggest that there may be a general increase in excitability of the vasomotor neurons in the medulla of the hypertensive rats.


1986 ◽  
Vol 64 (7) ◽  
pp. 1023-1026 ◽  
Author(s):  
B. Y. Ong ◽  
C. MacIntyre ◽  
D. Bose ◽  
R. J. Palahniuk

The cerebral blood flow of newborn lambs at reduced and elevated arterial blood pressures, induced by intravenous infusion of sodium nitroprusside and phenylephrine hydrochloride as well as blood withdrawal and reinfusion, were compared. Both blood withdrawal and sodium nitroprusside infusion reduced mean arterial pressure from 83 to 60 mmHg (1 mmHg = 133 Pa). Reinfusion of blood increased arterial pressure to 94 mmHg. Phenylephrine hydrochloride infusion increased arterial pressure to 102 mmHg. The cerebral blood flows at corresponding arterial pressures were similar (coefficient of correlation = 0.88, P < 0.01). Cerebral blood flow before and after infusion of phenylephrine hydrochloride and sodium nitroprusside into the brain via the carotid artery did not change. The results indicate that blood-borne phenylephrine hydrochloride and sodium nitroprusside, in concentrations that would alter arterial blood pressure significantly from its resting level, do not change cerebral blood flow directly.


1995 ◽  
Vol 78 (1) ◽  
pp. 101-111 ◽  
Author(s):  
J. M. Lash ◽  
H. G. Bohlen

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.


1987 ◽  
Vol 104 (3-4) ◽  
pp. 243-250 ◽  
Author(s):  
Maria Hillerdal ◽  
Erik Borg ◽  
Berit Engstrom ◽  
Elisabeth Hultcrantz

1987 ◽  
Vol 253 (4) ◽  
pp. H980-H984 ◽  
Author(s):  
M. A. Cierpial ◽  
R. McCarty

The role of the maternal environment in the development of hypertension in spontaneously hypertensive (SHR) rats was evaluated using the technique of reciprocal cross fostering. Litters of SHR and Wistar-Kyoto (WKY) normotensive pups were either reared by their natural mothers, in fostered to mothers of the same strain, or cross fostered to mothers of the opposite strain shortly after birth. Litters were weaned at 21 days of age, at which time all pups were weighed. At 18-20 wk of age, resting mean arterial blood pressures (MAP) and heart rates were determined for male subjects from the six groups (2 strains X 3 rearing conditions) via an indwelling tail artery catheter. At weaning, SHR animals weighed less than WKY animals. SHRs fostered to WKY mothers were significantly heavier than control SHRs, and WKYs fostered to SHR mothers were significantly lighter than WKY controls at weaning. These body weight differences were also evident in adulthood. Cross fostering SHR pups to normotensive WKY mothers resulted in a dramatic reduction in resting MAP measured in adulthood. Conversely, cross fostering WKY pups to SHR mothers had no measurable effect on adult resting MAP. We propose that an interaction between characteristics of the SHR maternal environment and a genetic susceptibility in SHR pups is essential in triggering the full expression of the hypertensive phenotype in this animal model of human essential hypertension.


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