Primary versus secondary structural changes of the blood vessels in hypertension

1985 ◽  
Vol 63 (4) ◽  
pp. 392-401 ◽  
Author(s):  
Robert M. K. W. Lee ◽  
John S. Smeda
Keyword(s):  
Blood Pressure ◽  
Blood Vessels ◽  
Structural Changes ◽  
Vascular Wall ◽  
Wall Thickening ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Pressure Independent ◽  
Hypertension Development

Various researchers have hypothesized that the thickening of the vascular wall plays an important role in the maintenance of hypertension. Such an alteration can increase the vascular resistance by exerting two effects. A thickened vascular wall could occlude the lumen of the blood vessel and (or) cause the artery to hyperreact to contractile stimuli. Until recently, it has been a general conclusion that such alterations were a secondary adaptation produced by the elevation of blood pressure. Consistent with this view, certain classes of larger arteries do exhibit a thickened vascular wall late during hypertension development and such changes can be prevented from occurring by antihypertensive treatment. However, recent studies involving the mesenteric and renal arteries of Wistar-Kyoto spontaneously hypertensive rats have shown that wall thickening of the vasculature occurs prior to hypertension development and is present even under conditions where the blood pressure has been normalized throughout the animal's life. These latter observations suggest that some structural alterations in the blood vessels observed in hypertension are pressure independent and could be of etiological importance in the initiation of hypertension.

Blood pressure and heart rate development in young spontaneously hypertensive rats

1998 ◽  
Vol 274 (3) ◽  
pp. H794-H800 ◽  
Author(s):  
Jeffrey G. Dickhout ◽  
Robert M. K. W. Lee
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Body Weight ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Genetic Trait ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Hypertension Development ◽  
Rate Development

The course of hypertension development in young spontaneously hypertensive rats (SHR) was studied by the measurement of changes in systolic blood pressure (BP), body weight, and heart rate (HR) at 2, 3, 4, and 6 wk of age. To achieve this, we compared inbreeding lines of SHR and Wistar-Kyoto rats (WKY) to determine if differences in BP, body weight, or HR were present among inbreeding lines of the same strain or between strains. The effect of these differences on the eventual level of BP was then assessed. We found that BP began to diverge between SHR and WKY at 4 wk of age. Significant differences in systolic BP (24 mmHg) between SHR inbreeding lines at 4 wk of age did not affect the BP at 8 wk (172 vs. 170 mmHg). Pulse pressure was significantly higher in SHR than in WKY at 4 wk of age. HR was elevated in SHR over age-matched WKY at 3 wk of age and positively correlated to the level of BP attained by individual animals at 6 wk ( P = 0.037). Moreover, WKY inbreeding lines showing elevated HR developed higher BP (145 vs. 127 mmHg) at 10–12 and 20 wk of age. The prehypertensive tachycardia in SHR was investigated further and found to result from an increased intrinsic HR. Because HR at 3 wk is a genetic trait that can be partitioned into inbreeding lines, and inbreeding lines most expressive of this trait showed the highest eventual BP, we conclude that prehypertensive tachycardia may be an important first step during hypertension development in SHR. Moreover, early elevations in HR are highly predictive ( r = 0.41) of hypertension occurrence in the animal population studied.

Is Arterial Media Hypertrophy in Spontaneously Hypertensive Rats a Consequence of or a Cause for Hypertension?

1980 ◽  
Vol 59 (s6) ◽  
pp. 331s-333s ◽  
Author(s):  
K. J. Henrichs ◽  
T.H. Unger ◽  
K. H. Berecek ◽  
D. Ganten
Keyword(s):  
Blood Pressure ◽  
High Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Structural Changes ◽  
Peripheral Resistance ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
The Media ◽  
Wistar Kyoto ◽  
Genetically Determined

1. The increased peripheral resistance observed in established hypertension has been attributed to structural changes in the resistance vessels, which are considered to be due mainly to medial hypertrophy. This study was undertaken to examine the possiblity that structural changes in the arterial bed are genetically determined and may be causative factors in the development of high blood pressure in the spontaneously hypertensive rat. 2. The wall dimensions of aorta, renal artery and intrarenal arteries down to a distended diameter of 35 μm were studied: (a) in 14-week-old spontaneously hypertensive rats; (b) in age- and sex-matched spontaneously hypertensive rats which had been treated with captopril for two generations and had been normotensive during their complete life span; (c) in normotensive Wistar-Kyoto control rats. 3. Cross-sectional areas of the media were increased in the hypertensive rats in comparison with ‘normotensive spontaneously hypertensive rats’ and Wistar-Kyoto rats. Increased numbers of smooth muscle cells were found in the major arteries of hypertensive animals. 4. These results indicate that hypertrophy of the media is a consequence of high blood pressure rather than a genetically determined pathogenetic factor for the development of hypertension in spontaneously hypertensive rats.

Effects of dietary Ca2+ on erythrocyte Na+-transport systems in spontaneously hypertensive rats

1991 ◽  
Vol 81 (1) ◽  
pp. 107-112 ◽  
Author(s):  
K. Fujito ◽  
M. Yokomatsu ◽  
N. Ishiguro ◽  
H. Numahata ◽  
Y. Tomino ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Transport Systems ◽  
Hypertensive Rats ◽  
Na Transport ◽  
Spontaneously Hypertensive ◽  
Na Pump ◽  
Wistar Kyoto ◽  
Increased Activity ◽  
Regulation Of Blood Pressure

1. The purpose of this study was to determine the effect of dietary Ca2+ intake on blood pressure and erythrocyte Na+ transport in spontaneously hypertensive rats. 2. Spontaneously hypertensive rats and Wistar-Kyoto rats were fed diets with three different Ca2+ contents, 0.1% (low-Ca2+ diet), 0.6% (normal-Ca2+ diet) and 4.0% (high-Ca2+ diet), between 6 and 20 weeks of age. At 20 weeks of age, the levels of erythrocyte Na+ efflux, as well as Na+ and K+ contents in erythrocytes, were measured. 3. On the low-Ca2+ diet, spontaneously hypertensive rats showed an enhancement of hypertension. Conversely, on the high-Ca2+ diet, they showed an attenuation of the increase in blood pressure. Spontaneously hypertensive rats had a lower erythrocyte Na+ content and increased activity of the Na+ pump at higher levels of dietary Ca2+. Passive Na+ permeability and Na+-K+ co-transport were similar in spontaneously hypertensive rats on the low-, normal- and high-Ca2+ diets. There were no significant differences in blood pressure and in Na+ pump activity in WKY on the three different diets. 4. It is concluded that dietary Ca2+ might affect the regulation of blood pressure in spontaneously hypertensive rats by changing the activity of Na+ pump in the cell membrane.

Increased Pressor Responsiveness to Enkephalin in Spontaneously Hypertensive Rats: The Role of Vasopressin

1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Hypertensive Rats ◽  
Methionine Enkephalin ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.

Metformin decreases plasma insulin levels and systolic blood pressure in spontaneously hypertensive rats

1994 ◽  
Vol 267 (4) ◽  
pp. H1250-H1253 ◽  
Author(s):  
S. Verma ◽  
S. Bhanot ◽  
J. H. McNeill
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Insulin ◽  
Metformin Treatment ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Insulin Levels ◽  
Plasma Insulin Levels ◽  
Wistar Kyoto

To determine the relationship between hyperinsulinemia and hypertension in spontaneously hypertensive rats (SHR), the antihyperglycemic agent metformin was administered to SHR and their Wistar-Kyoto (WKY) controls, and its effects on plasma insulin levels and blood pressure were examined. Five-week-old rats were started on oral metformin treatment (350 mg.kg-1.day-1, which was gradually increased to 500 mg.kg-1.day-1 over a 2-wk period). Metformin treatment caused sustained decreases in plasma insulin levels in the SHR (27.1 +/- 2.3 vs. untreated SHR 53.5 +/- 2.7 microU/ml, P < 0.001) without having any effect in the WKY (30.7 +/- 2.2 vs. untreated WKY 37.8 +/- 1.6 microU/ml, P > 0.05). The treatment did not affect the plasma glucose levels in any group. Metformin treatment also attenuated the increase in systolic blood pressure in the SHR (157 +/- 6.0 vs. untreated SHR 196 +/- 9.0 mmHg, P < 0.001) but had no effect in the WKY (134 +/- 3 vs. untreated WKY 136 +/- 4 mmHg, P > 0.05). Furthermore, raising plasma insulin levels in the metformin-treated SHR to levels that existed in the untreated SHR reversed the effect of metformin on blood pressure (189 +/- 3 vs. untreated SHR 208 +/- 5.0 mmHg, P > 0.05). These findings suggest that either hyperinsulinemia may contribute toward the increase in blood pressure in the SHR or that the underlying mechanism is closely associated with the expression of both these disorders.

Contribution of Vascular Nitric Oxide to Basal Blood Pressure in Conscious Spontaneously Hypertensive Rats and Normotensive Wistar Kyoto Rats

1995 ◽  
Vol 89 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Naoyoshi Minami ◽  
Yutaka Imai ◽  
Jun-Ichiro Hashimoto ◽  
Keishi Abe
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Methyl Ester ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Basal Blood Pressure ◽  
Wistar Kyoto

1. The aim of this study was to clarify the extent to which vascular nitric oxide contributes to basal blood pressure in conscious spontaneously hypertensive rats and normotensive Wistar Kyoto rats. 2. The contribution of vascular nitric oxide to maintenance of blood pressure was estimated by measuring the pressor response to an intravenous injection of nitric oxide synthase inhibitor, Nω-l-arginine methyl ester, given after serial injections of captopril, vasopressin V1-receptor antagonist (V1-antagonist) and ganglion blocker (pentolinium) in conscious spontaneously hypertensive and Wistar Kyoto rats aged 20–28 weeks. To estimate the ‘amplifier property’ of hypertrophied vasculature in spontaneously hypertensive rats, which is known to modulate pressor responses, the lower blood pressure plateau after serial injections of captopril, V1-antagonist and pentolinium and the maximum blood pressure elicited by subsequent injection of increasing doses of phenylephrine were also measured. 3. The serial injections of captopril, V1-antagonist and pentolinium decreased mean arterial pressure from 164 ± 9 mmHg to 67 ± 2 mmHg and from 117 ± 2 mmHg to 49 ± 1 mmHg in spontaneously hypertensive and Wistar Kyoto rats respectively. The subsequent injection of Nω-l-arginine methyl ester restored mean arterial pressure almost to its control levels in both spontaneously hypertensive and Wistar Kyoto rats. The absolute changes in mean arterial pressure elicited by Nω-l-arginine methyl ester were significantly greater in spontaneously hypertensive than in Wistar Kyoto rats (P < 0.01), but there was no significant difference in the responses to Nω-l-arginine methyl ester when they were expressed as percentages of either the lower blood pressure plateau or maximum blood pressure. 4. These results indicate that basal blood pressure in both spontaneous hypertensive and Wistar Kyoto rats is maintained by a balance between vascular nitric oxide and major pressor systems. They also suggest that the vasodilatory effect of vascular nitric oxide does not differ between spontaneously hypertensive and Wistar Kyoto rats, and that the increased pressor effect of Nω-l-arginine methyl ester in spontaneously hypertensive rats is due to a vascular amplifier mechanism.

Ca2+ sensitization and Ca2+ entry in the control of blood pressure and adrenergic vasoconstriction in conscious Wistar–Kyoto and spontaneously hypertensive rats

2013 ◽  
Vol 31 (10) ◽  
pp. 2025-2035 ◽  
Author(s):  
Michal Behuliak ◽  
Mária Pintérová ◽  
Michal Bencze ◽  
Miriam Petrová ◽  
Silvia Líšková ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Hypertension transmitted by kidneys from stroke-prone spontaneously hypertensive rats

1989 ◽  
Vol 257 (2) ◽  
pp. F197-F203 ◽  
Author(s):  
R. Rettig ◽  
H. Stauss ◽  
C. Folberth ◽  
D. Ganten ◽  
B. Waldherr ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Transplantation ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Renin ◽  
F1 Hybrids ◽  
Hypertensive Rats ◽  
Plasma Urea ◽  
Spontaneously Hypertensive ◽  
Major Function ◽  
Wistar Kyoto

We determined whether transplantations of kidneys from stroke-prone spontaneously hypertensive rats (SPSHR) and from normotensive Wistar-Kyoto rats (WKY) alter blood pressure in renal graft recipients. Kidneys taken from seven male SPSHR and seven male WKY rats (blood pressure 186 +/- 4.8 and 111 +/- 3.7 mmHg, respectively) at the age of 20 wk were transplanted, using microsurgical techniques, to bilaterally nephrectomized age-matched male F1 hybrids (blood pressure 136 +/- 2.6 and 138 +/- 6.3 mmHg, respectively) bred from SPSHR and WKY parents. After renal transplantation, blood pressure in recipients of SPSHR kidneys rose to 146 +/- 11.8 (week 2), 163 +/- 16.4 (week 3), 192 +/- 17.1 (week 4), 222 +/- 17.7 (week 5), 221 +/- 12.6 (week 6), 218 +/- 20.3 (week 7), and 239 +/- 9.2 mmHg (week 8). There was no significant change in blood pressure in recipients of WKY kidneys. All rats recovered rapidly from surgery. After renal transplantation, there was a significant increase in daily water intake, a decrease in plasma renin activity, and a slight rise in plasma urea concentration. Our data show that transplantation of kidneys from adult SPSHR causes hypertension in normotensive recipients, indicating a major function for the kidney in SPSHR hypertension.

scholarly journals Duration of Electrically Induced Atrial Fibrillation Is Augmented by High Voltage of Stimulus with Higher Blood Pressure in Hypertensive Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Tomomi Nagayama ◽  
Yoshitaka Hirooka ◽  
Akiko Chishaki ◽  
Masao Takemoto ◽  
Yasushi Mukai ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Blood Pressure ◽  
Arterial Pressure ◽  
High Voltage ◽  
Spontaneously Hypertensive Rats ◽  
Low Voltage ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Stimulus ◽  
Wistar Kyoto

Objective.Many previous clinical studies have suggested that atrial fibrillation (AF) is closely associated with hypertension. However, the benefits of antihypertensive therapy on AF are still inconsistent, and it is necessary to explore the factors augmenting AF in hypertensive rats. The aim of the present study was to investigate the correlation between arterial pressure or voltage stimulus and to the duration of electrically induced AF in normotensive or hypertensive rats.Methods.AF was reproducibly induced by transesophageal atrial burst pacing in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). We did the burst pacing at high (20 V) or low (5 V) voltage.Results.Duration of AF did not correlate with systolic blood pressure (SBP) and stimulus voltage in WKY. However, only in SHR, duration of AF with high stimulus voltage significantly correlated with SBP and was significantly longer in high than in low voltage stimulus.Discussion and Conclusion.Duration of AF is augmented by high voltage stimulus with higher blood pressure in SHR.

Plasma Concentrations of Catecholamines in Two Strains of Spontaneously Hypertensive Rats at Different Ages

1981 ◽  
Vol 61 (s7) ◽  
pp. 199s-202s ◽  
Author(s):  
P. Ferrari ◽  
G. B. Picotti ◽  
E. Minotti ◽  
G. P. Bondiolotti ◽  
A. M. Caravaggi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Concentrations ◽  
Plasma Catecholamine ◽  
Hypertensive Rats ◽  
Adult Rats ◽  
Plasma Adrenaline ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Normotensive Strain ◽  
Noradrenaline And Adrenaline

1. Blood pressure was measured and plasma levels of noradrenaline and adrenaline were determined radioenzymatically under basal conditions and after 10% blood volume reduction in blood drawn through catheters previously implanted in young and adult rats of two different genetically hypertensive strains: the Kyoto strain (SHR) and the Milan strain (MHS), and in their respective controls: Wistar—Kyoto strain (WKY) and Milan normotensive strain (MNS). 2. Under basal conditions no differences were observed between plasma noradrenaline and adrenaline levels in SHR and MHS rats and in the controls, at any age. Haemorrhage produced a greater fall in the blood pressure (P &lt; 0.01) of young and adult hypertensive strains (SHR-MHS) than in WKY and MNS rats, and a greater rise in plasma adrenaline (P &lt; 0.01). 3. These results suggest that: (a) there may be differences in involvement of the sympathetic nervous system in the pathogenesis of hypertension in SHR and MHS rats but not such as to cause differences in plasma catecholamine levels in either young or adult rats; (b) haemorrhage activates the sympatho—adrenal systems more in SHR and MHS rats, than in controls, and the greater percentage fall in blood pressure is probably due to a difference in reflex venoconstriction.

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