Sympathetic vascular tone in spontaneous hypertension of rats

Schömig, Albert; Dietz, Rainer; Rascher, Wolfgang; Lüth, J. B.; Mann, Johannes F.E.; Schmidt, Martin; Weber, João Batista Blessmann

doi:10.1007/bf01477464

Cited by 38 publications

(7 citation statements)

References 23 publications

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“…Here ganglionic blockade by injection of hexamethonium caused equal percentage decreases in blood pressure in SHRs and WKYs. Furthermore, chemical denervation of SHRs and WKYs at birth does not prevent the blood pressure rising to levels above those of denervated WKYs [Schomig et al, 1978], and similar results were obtained with the New Zealand strain of genetically hypertensive rat [Clark et al, 1978] . Thus, although neurogenic mecha nisms may be involved in the development of hypertension in the SHR, increased TPR in SHRs also appears to be both initiated and maintained by non-ncurogenic mechanisms.…”

Section: Evidence For Increased External Activation O F the Shr Vascusupporting

confidence: 67%

Do Resistance Vessel Abnormalities Contribute to the Elevated Blood Pressure of Spontaneously-Hypertensive Rats?

Mulvany¹

1983

J Vasc Res

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This review summarizes some of the evidence pointing to the existence of vascular abnormalities in the spontaneously hypertensive rat (SHR) and the extent to which such abnormalities could be responsible for the elevated blood pressure in this animal. Compared with its genetic normotensive control, the Wistar-Kyoto rat (WKY), the adult SHR has an increased total peripheral resistance (TPR). Many factors appear to contribute to the increased TPR, including an active rarefication of the vascular bed and a general constriction of the vasculature. There is evidence that the general constriction is due to structural differences in the resistance vessels, to abnormally high activation levels (i.e. increased sympathetic nerve activity), and to abnormal excitation-contracting coupling within the vasculature itself (i.e. increased noradrenaline sensitivity of the vascular smooth muscle cells). Age studies and studies of the effects of antihypertensive treatment suggest that both structural and excitation-contraction abnormalities may be present before the onset of hypertension.

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Section: Evidence For Increased External Activation O F the Shr Vascusupporting

confidence: 67%

Do Resistance Vessel Abnormalities Contribute to the Elevated Blood Pressure of Spontaneously-Hypertensive Rats?

Mulvany¹

1983

J Vasc Res

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“…During hypertension the amplitude of the constrictor response of pial arteries to stimulation of the superior cervical ganglion did not increase, which contradict published data [6,8]. In both rat groups, the amplitude of the constrictor response was 10-20% of the initial diameter.…”

Section: Resultscontrasting

confidence: 56%

Neurogenic vasoconstriction of pial arterial vessels of various branching orders in normotensive and spontaneously hypertensive rats

2006

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Intravital television microscopy was employed to study the reaction of pial arteries in normotensive and spontaneously hypertensive rats to stimulation of the superior cervical ganglion. The amplitude of constrictor response was similar in WKY and SHR animals. Under conditions of normal arterial pressure and arterial hypertension, the maximum constrictor effect was attained due to equal involvement of the arteries from all generations in the normotensive rats and predominant constriction of the precortical arterioles in SHR animals.

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“…We therefore have to consider the possibility that AVP, similar to the adrenergic nervous system and to opioid peptides, may not only activate pressor but also depressor mechanisms. The high blood pressure in SHRDI rats might then not occur "despite" the fact that AVP is absent, but this defect may even contribute to the development of high blood pressure, since other pressor stimuli such as an increased sympathetic tone 32 remain unopposed in the AVP-deficient SHRDI rats.…”

Section: -127mentioning

confidence: 99%

Development of a new strain of spontaneously hypertensive rats homozygous for hypothalamic diabetes insipidus.

Ganten¹,

Rascher²,

Lang³

et al. 1983

Hypertension

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SUMMARY The aim of the present study was to investigate whether the presence of arginine vasopressin (AVP) is necessary for the establishment of high blood pressure in spontaneously hypertensive rats (SHR). For this purpose we crossbred SHR of the stroke-prone substrain (SHRSP) with rats homozygous for hypothalamic diabetes insipidus of the Brattleboro strain (DI) which are unable to synthetize AVP. The successful introduction of the DI gene into the SHRSP strain (SHRDI) was demonstrated by the following observations: In 10-month-old rats, water intake was similarly elevated in SHRDI as in DI rats (137 ± 6.5 vs 125 ± 10.5 ml per 24 hours). AVP was undetectable in the plasma, in the hypothalamus, and in the pituitary of SHRDI and DI rats. Urine osmolality and urinary concentration of sodium and potassium were markedly reduced. SHRDI and DI did not adequately concentrate their urine during an 8-hour period of water deprivation, but both strains of rats responded well with a fall in urine output and a rise in urine osmolality to subcutaneous administration of the non-pressor analog of AVP, DDAVP. Mean arterial blood pressure was markedly increased in SHRDI as well as in SHRSP (184 ± 9.7 vs 197 ± 5.2 mm Hg). Thus, we have developed a new line of spontaneously hypertensive rats homozygous for hypothalamic diabetes insipidus. From this finding it is concluded that AVP is not essential for the development and maintenance of spontaneous hypertension of rats. Authors' Note: The trivial name "Heidelberg Hypertensive Drinkers" (HHD) has been proposed for these rats.AVP-antiserum lowered blood pressure in these rats, it has been concluded that AVP plays a role in the maintenance of high blood pressure in SHRSP. 2In contrast to these results, we have recently found that plasma levels of AVP were below normal in SHRSP at 6, 9, and 12 weeks of age; they were higher than in age-matched Wistar-Kyoto rats (WKY) only in SHRSP older than 24 weeks of age.3 -4 Intravenous administration of specific vasopressor AVP antagonists 3 had no significant influence on mean arterial pressure'-4 and on cardiac output or total peripheral resistance. 4 Furthermore, reduced contents of AVP were found in the hypothalamus, in the brain stem, and in the amygdala of SHRSP.^ From these results we have concluded that circulating AVP does not contribute to the development and maintenance of high blood pressure. The question whether AVP is involved in the pathogenesis of spontaneous hypertension of rats'-2 or not 3 -4 is therefore unresolved.

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Sympathetic vascular tone in spontaneous hypertension of rats

Cited by 38 publications

References 23 publications

Do Resistance Vessel Abnormalities Contribute to the Elevated Blood Pressure of Spontaneously-Hypertensive Rats?

Do Resistance Vessel Abnormalities Contribute to the Elevated Blood Pressure of Spontaneously-Hypertensive Rats?

Neurogenic vasoconstriction of pial arterial vessels of various branching orders in normotensive and spontaneously hypertensive rats

Development of a new strain of spontaneously hypertensive rats homozygous for hypothalamic diabetes insipidus.

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