Enhanced response of arterioles to oxygen during development of hypertension in SHR

1986 ◽  
Vol 250 (5) ◽  
pp. H761-H764 ◽  
Author(s):  
J. H. Lombard ◽  
M. E. Hess ◽  
W. J. Stekiel
Keyword(s):  
Skeletal Muscle ◽  
Vascular Resistance ◽  
Local Control ◽  
Fourth Order ◽  
Spontaneously Hypertensive Rat ◽  
Control Mechanisms ◽  
Cremaster Muscle ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

The goal of this study was to assess the possible role of O2-related local control mechanisms in contributing to an elevated skeletal muscle resistance during the development of hypertension in the spontaneously hypertensive rat (SHR). Diameters of first- (1A), second- (2A), third- (3A), and fourth-order (4A) arterioles were measured by television microscopy in the cremaster muscle of SHR in the early (4- to 6-wk-old) and rapidly developing (8- to 9-wk-old) stages of hypertension and in age-matched normotensive Wistar-Kyoto (WKY) controls. Active neurogenic tone was blocked by superfusing the tissue with 0.1 microgram/ml tetrodotoxin. When superfusion solution PO2 was elevated by changing the gas equilibration mixture from 0 to 5% O2, neurally blocked 3A and 4A of SHR exhibited a significantly greater constriction and a higher incidence of complete closure than those of their age-matched WKY controls. However, there were no significant differences in the constriction of larger arterioles (1A and 2A) in response to elevated superfusion solution PO2. The results suggest that O2-related local control mechanisms could contribute to constriction and closure of small arterioles and to an elevated skeletal muscle vascular resistance early in the development of hypertension in SHR

Microvascular rarefaction in spontaneously hypertensive rat cremaster muscle

1981 ◽  
Vol 241 (3) ◽  
pp. H306-H310 ◽  
Author(s):  
I. I. Chen ◽  
R. L. Prewitt ◽  
R. F. Dowell
Keyword(s):  
Surface Area ◽  
Fourth Order ◽  
Unit Volume ◽  
Spontaneously Hypertensive Rat ◽  
Absolute Number ◽  
Cremaster Muscle ◽  
Vascular Effects ◽  
Spontaneously Hypertensive ◽  
Vessel Length ◽  
Wistar Kyoto

We have investigated the neural and local vascular effects on vessel length and surface area per unit volume in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) by quantitative stereology. Fourteen SHR and 14 KWY (70-130 g) were anesthetized with chloralose-urethan, and the cremaster muscle was exposed for microscopic observation. The large arterioles entering the muscle were termed the first order, and consecutive branches were termed second-, third-, and fourth-order arterioles. The data were collected in three consecutive states: innervated, denervated, and vasodilated with nitroprusside. The third- and fourth-order arteriole and capillary lengths per unit volume in the SHR were less than those of the WKY in all three states. The vessel surface area per unit volume was also reduced in the SHR. Denervation and sodium nitroprusside (Nipride) resulted in larger percent increases in vessel length and surface area in the SHR than in the WKY. We conclude that in the SHR cremaster muscle there are fewer terminal arterioles and capillaries anatomically present, and, under resting conditions, a greater percentage but similar absolute number of them are closed to flow.

Role of adenosine in noradrenergic neurotransmission in spontaneously hypertensive rats

1987 ◽  
Vol 253 (4) ◽  
pp. H909-H918 ◽  
Author(s):  
E. K. Jackson
Keyword(s):  
Plasma Levels ◽  
Spontaneously Hypertensive Rat ◽  
Base Line ◽  
Inhibitory Effects ◽  
Spontaneously Hypertensive ◽  
Vascular Responses ◽  
Rat Mesentery ◽  
Wistar Kyoto

The purpose of this study was to compare the in vivo role of adenosine as a modulator of noradrenergic neurotransmission in the spontaneously hypertensive rat (SHR) and Wistar-Kyoto control rat (WKY). In the in situ blood-perfused rat mesentery, vascular responses to periarterial (sympathetic) nerve stimulation (PNS) and to exogenous norepinephrine (NE) were enhanced in SHR compared with WKY. In both SHR and WKY, vascular responses to PNS were more sensitive to inhibition by adenosine than were responses to NE. At matched base-line vascular responses, compared with WKY, SHR were less sensitive to the inhibitory effects of adenosine on vascular responses to PNS, but SHR and WKY were equally sensitive with respect to adenosine-induced inhibition of responses to NE. Antagonism of adenosine receptors with 1,3-dipropyl-8-p-sulfophenylxanthine shifted the dose-response curve to exogenous adenosine sixfold to the right yet did not influence vascular responses to PNS or NE in either SHR or WKY. Furthermore, PNS did not alter either arterial or mesenteric venous plasma levels of adenosine in SHR or WKY, and plasma levels of adenosine in both strains were always lower than the calculated threshold level required to attenuate neurotransmission. It is concluded that in vivo 1) exogenous adenosine interferes with noradrenergic neurotransmission in both SHR and WKY; 2) SHR are less sensitive to the inhibitory effects of exogenous adenosine on noradrenergic neurotransmission than are WKY; 3) endogenous adenosine does not play a role in modulating neurotransmission in either strain under the conditions of this study; and 4) enhanced noradrenergic neurotransmission in the SHR is not due to defective modulation of neurotransmission by adenosine.

Age-dependent regulation of vasopressin V1a receptors in preglomerular vessels from the spontaneously hypertensive rat

2004 ◽  
Vol 286 (5) ◽  
pp. F997-F1003 ◽  
Author(s):  
Øyvind B. Vågnes ◽  
Frank H. Hansen ◽  
Rolf E. F. Christiansen ◽  
Camilla Gjerstad ◽  
Bjarne M. Iversen
Keyword(s):  
Spontaneously Hypertensive Rat ◽  
Mrna Level ◽  
Cytosolic Calcium ◽  
Receptor Expression ◽  
Receptor Protein ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Renal Vascular ◽  
Insight Into

Experiments were performed to get insight into the role of AVP receptor V1a regulation with age, i.e., during development and maintenance of high blood pressure. Previous studies showed an increased gene expression and renal vascular response to AVP in young spontaneously hypertensive rats (SHR). The age regulation of the V1a receptor was examined in preglomerular vessels from 5-, 10-, 20-, and 70-wk-old SHR using normotensive Wistar-Kyoto rats (WKY) as controls. Real-time PCR and ligand binding were used for analysis of receptor expression, and the change in cytosolic calcium concentration during stimulation of isolated preglomerular vessels with AVP was studied. Studies showed an increase of the V1a receptor protein and mRNA from 5-and 10-wk-old SHR compared with vessels from 20- and 70-wk-old SHR. In 5-wk-old SHR receptor density was 84 ± 13 fmol/mg protein, and 38 ± 11 fmol/mg protein in 70-wk-old SHR ( P < 0.05). mRNA in the 5- and 70-wk-old SHR was 15,854 ± 629 and 3,181 ± 224 V1a mRNA/108 18S ribosomal RNA, respectively ( P < 0.001). Values from WKY at all ages were similar to 20- and 70-wk-old SHR. During stimulation with AVP, the change in cytosolic calcium in vessels from 5-wk-old SHR increased 234 ± 59 nM, whereas the increase was 89 ± 9 nM in 70-wk-old SHR ( P = 0.03). These results indicate that the V1a receptor is increased at protein and mRNA level during development of hypertension in SHR but is normalized when hypertension is established.

Epitranscriptomic mechanisms of N6-methyladenosine methylation regulating mammalian hypertension development by determined spontaneously hypertensive rats pericytes

Epigenomics ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 1359-1370 ◽  
Author(s):  
Qingbin Wu ◽  
Xiaochen Yuan ◽  
Ruiqin Han ◽  
Honggang Zhang ◽  
Ruijuan Xiu
Keyword(s):  
High Throughput Sequencing ◽  
Spontaneously Hypertensive Rat ◽  
Biological Processes ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Sequence Region ◽  
Wistar Kyoto Rat ◽  
Wistar Kyoto ◽  
Hypertension Development

Aim: Pericytes maintain homeostatic functions in the blood–brain barrier. N6-methyladenosine (m6A) is critical for various biological processes, but the role of mRNA m6A methylation in hypertension has not been fully elucidated. Methods: The m6A methylation levels of Wistar Kyoto rat pericytes and spontaneously hypertensive rat pericytes were detected via m6A high-throughput sequencing. Results: The m6A methylations were more enriched in the coding sequence region, 3′UTR and 5′UTR of mRNAs, with the m6A motifs being relatively conserved across the different conditions investigated. The average m6A abundance of spontaneously hypertensive rat pericytes exhibited global reductions in the pericytes. Conclusion: This study revealed the m6A landscapes and identified an epitranscriptomic mechanism during the development of mammalian hypertension.

Segmental renal vascular resistance in the spontaneously hypertensive rat

1982 ◽  
Vol 242 (6) ◽  
pp. H961-H966 ◽  
Author(s):  
C. H. Hsu ◽  
J. H. Slavicek ◽  
T. W. Kurtz
Keyword(s):  
Vascular Resistance ◽  
Spontaneously Hypertensive Rat ◽  
Renal Vascular Resistance ◽  
Hypertensive Rats ◽  
Mean Values ◽  
Spontaneously Hypertensive ◽  
Microsphere Method ◽  
Wistar Kyoto ◽  
Renal Vascular ◽  
Arteriolar Diameter

Renal hemodynamics were studied during different stages of development of hypertension in unanesthetized spontaneously hypertensive rats (SHR). In SHR at 4 wks of age mean arterial pressure (MAP) was higher than in age-matched Wistar Kyoto rats (WKY); however, renal blood flow (RBF) and renal vascular resistance (RVR) were not different between these two groups. Mean values of RVR and MAP in 8- and 12-wk-old SHR were significantly greater than those of age-matched WKY. Both RBF of 8- and 12-wk-old SHR were significantly lower than the corresponding values of WKY. Afferent arteriolar diameter (AAD) was measured with a microsphere method. AAD was not different between 4-wk-old SHR and WKY; however, the AAD of 8-wk-old (16.3 +/- 0.23 micrometers, n = 5) and 12-wk-old (17.4 +/- 0.48, n = 5) SHR were significantly smaller than those of respective control WKY (17.3 +/- 0.34, n = 4, P less than 0.05; 19.3 +/- 0.12, n = 5, P less than 0.01). Calculated preglomerular (Rpre) and postglomerular resistances (Rpost) of 12-wk-old SHR were increased 96 and 129% when compared with respective segmental resistances of the control WKY. The decrease in AAD of 12-wk-old SHR was sufficient to account for a 33% increase in Rpre. After the rats were treated with hydralazine (0.5 mg/kg iv), MAP, RBF, and RVR of SHR were not different from the control WKY values. Rpre and Rpost of SHR were substantially decreased; however, vasodilation occurred at vessels proximal and distal to the afferent arteriole because AAD was not altered. Our results indicate that increased RVR in SHR involves increases in Rpre and Rpost.

Renal interstitial hydrostatic pressure and ANF in exaggerated natriuresis of the SHR

1990 ◽  
Vol 258 (6) ◽  
pp. R1380-R1385 ◽  
Author(s):  
A. A. Khraibi ◽  
D. M. Heublein ◽  
J. C. Burnett ◽  
F. G. Knox
Keyword(s):  
Hydrostatic Pressure ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Spontaneously Hypertensive Rat ◽  
Intact Control ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
High Level ◽  
Expansion Period

The Okamoto spontaneously hypertensive rat (SHR) has exaggerated natriuretic and diuretic responses to acute volume expansion in comparison with the Wistar-Kyoto (WKY) rat. The objective of these experiments was to determine the role of renal interstitial hydrostatic pressure (RIHP) and atrial natriuretic factor (ANF) in these natriuretic and diuretic responses of the SHR and the WKY rat. Two groups each of SHRs and WKY rats were used in this study. In one group of each, both kidneys were acutely decapsulated, and in the remaining two groups the renal capsules were left intact (control). In both control SHR (n = 6) and WKY (n = 7) groups, volume expansion was associated with a significant increase in RIHP (from 5.0 +/- 0.5 to 7.1 +/- 0.6 mmHg in SHR group and from 6.0 +/- 0.5 to 9.4 +/- 0.3 mmHg in WKY rat group) and a high level of plasma ANF (PANF). The increase in RIHP was significantly lower in the control SHR group compared with that of control WKY rat group (2.1 +/- 0.4 vs. 3.5 +/- 0.3 mmHg; P less than 0.05), whereas PANF was significantly higher in the SHR group (848 +/- 151 pg/ml) compared with that of the WKY group (503 +/- 37 pg/ml) at the end of the volume-expansion period. When the increase in RIHP that occurs during volume expansion in the SHR is blunted by acute bilateral renal decapsulation, the natriuretic and diuretic responses are significantly attenuated despite levels of PANF that are similar to those measured in the control SHR group.(ABSTRACT TRUNCATED AT 250 WORDS)

Nonlinear analysis of BP signal. Can it detect malfunctions in BP control?

1996 ◽  
Vol 271 (2) ◽  
pp. H396-H403 ◽  
Author(s):  
Y. Almog ◽  
S. Eliash ◽  
O. Oz ◽  
S. Akselrod
Keyword(s):  
Spontaneously Hypertensive Rat ◽  
Surrogate Data ◽  
Cardiovascular Control ◽  
Control Mechanisms ◽  
Spontaneously Hypertensive ◽  
New Information ◽  
Wistar Kyoto Rat ◽  
Nonlinear Technique ◽  
Wistar Kyoto ◽  
Nonlinear Components

In the present study, our aim was to evaluate the applicability of the nonlinear technique to the investigation of cardiovascular control. We applied an approach known as the “surrogate data method” to test for nonlinear components in the blood pressure (BP) signal. Our results strongly indicate that there are nonlinear components in the BP time series taken from a Wistar-Kyoto rat (WKY), suggesting that the use of nonlinear methods may provide new information about the BP control system. We developed a procedure appropriate for the stable and reliable calculation of the Grassberger-Procaccia correlation dimension (D) of the arterial BP signal. The saturation value D was 5.48 +/- 0.30 for the WKY group and 5.92 +/- 0.26 for the spontaneously hypertensive rat (SHR) group, with P < 0.001. We also found that in the WKY group D displays a significant response to complete alpha 1 blockade and bleeding, whereas no response is observed in the SHR group. These results imply that differences in the control mechanisms may be detected by the nonlinear dynamics approach both under baseline conditions and when interfering with cardiovascular control.

scholarly journals Increases in plasma trans-EETs and blood pressure reduction in spontaneously hypertensive rats

2011 ◽  
Vol 300 (6) ◽  
pp. H1990-H1996 ◽  
Author(s):  
Houli Jiang ◽  
John Quilley ◽  
Anabel B. Doumad ◽  
Angela G. Zhu ◽  
John R. Falck ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rat ◽  
Blood Pressure Reduction ◽  
Maximal Velocity ◽  
Spontaneously Hypertensive ◽  
Cis And Trans Isomers ◽  
Wistar Kyoto Rat ◽  
Wistar Kyoto ◽  
Cis And Trans ◽  
Cis Isomer

Epoxyeicosatrienoic acids (EETs) are vasodilator, natriuretic, and antiinflammatory lipid mediators. Both cis- and trans-EETs are stored in phospholipids and in red blood cells (RBCs) in the circulation; the maximal velocity ( Vmax) of trans-EET hydrolysis by soluble epoxide hydrolase (sEH) is threefold that of cis-EETs. Because RBCs of the spontaneously hypertensive rat (SHR) exhibit increased sEH activity, a deficiency of trans-EETs in the SHR was hypothesized to increase blood pressure (BP). This prediction was fulfilled, since sEH inhibition with cis-4-[4-(3-adamantan-1-ylureido)cyclohexyloxy]benzoic acid (AUCB; 2 mg·kg−1·day−1 for 7 days) in the SHR reduced mean BP from 176 ± 8 to 153 ± 5 mmHg ( P < 0.05), whereas BP in the control Wistar-Kyoto rat (WKY) was unaffected. Plasma levels of EETs in the SHR were lower than in the age-matched control WKY (16.4 ± 1.6 vs. 26.1 ± 1.8 ng/ml; P < 0.05). The decrease in BP in the SHR treated with AUCB was associated with an increase in plasma EETs, which was mostly accounted for by increasing trans-EET from 4.1 ± 0.2 to 7.9 ± 1.5 ng/ml ( P < 0.05). Consistent with the effect of increased plasma trans-EETs and reduced BP in the SHR, the 14,15- trans-EET was more potent (ED50 10−10 M; maximum dilation 59 ± 15 μm) than the cis-isomer (ED50 10−9 M; maximum dilation 30 ± 11 μm) in relaxing rat preconstricted arcuate arteries. The 11,12-EET cis- and trans-isomers were equipotent dilators as were the 8,9-EET isomers. In summary, inhibition of sEH resulted in a twofold increase in plasma trans-EETs and reduced mean BP in the SHR. The greater vasodilator potency of trans- vs. cis-EETs may contribute to the antihypertensive effects of sEH inhibitors.

Enhanced renal sensitivity of the spontaneously hypertensive rat to urotensin II

2008 ◽  
Vol 295 (4) ◽  
pp. F1239-F1247 ◽  
Author(s):  
Alaa E. S. Abdel-Razik ◽  
Richard J. Balment ◽  
Nick Ashton
Keyword(s):  
Renal Function ◽  
Spontaneously Hypertensive Rat ◽  
Renal Medulla ◽  
Fractional Excretion ◽  
Urotensin Ii ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Hypertensive Rat ◽  
Fractional Excretion Of Sodium ◽  
Wistar Kyoto

Urotensin II (UII) has been implicated widely in cardiovascular disease. The mechanism(s) through which it contributes to elevated blood pressure is unknown, but its emerging role as a regulator of mammalian renal function suggests that the kidney might be involved. The aim of this study was to determine the effect of UII on renal function in the spontaneously hypertensive rat (SHR). UII infusion (6 pmol·min−1·100 g body wt−1) in anesthetized SHR and control Wistar-Kyoto (WKY) rats produced marked reductions in glomerular filtration rate (ΔGFR WKY, n = 7, −0.3 ± 0.1 vs. SHR, n = 7, −0.6 ± 0.1 ml·min−1·100 g body wt−1, P = 0.03), urine flow, and sodium excretion rates, which were greater in SHR by comparison with WKY rats. WKY rats also showed an increase in fractional excretion of sodium (ΔFENa; +0.6 ± 0.1%, P = 0.02) in contrast to SHR in which no such change was observed (ΔFENa −0.6 ± 0.2%). Blockade of the UII receptor (UT), and thus endogenous UII activity, with urantide evoked an increase in GFR which was greater in SHR (+0.3 ± 0.1) compared with WKY rats (+0.1 ± 0.1 ml·min−1·100 g body wt−1, P = 0.04) and was accompanied by a diuresis and natriuresis. UII and UT mRNA expression were greater in the renal medulla than the cortex of both strains; however, expression levels were up to threefold higher in SHR tissue. SHR are more sensitive than WKY to UII, which acts primarily to lower GFR thus favoring salt retention in this model of hypertension.

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