Aortic reactivity and electro‐physiology in normotensive rats, spontaneously hypertensive rats and rats made hypertensive with desoxycorticosterone plus salt

Massingham, R.; Shevde, S.

doi:10.1111/j.1476-5381.1971.tb07224.x

Cited by 9 publications

(6 citation statements)

References 2 publications

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“…This may indicate that structural changes in the vessels (8,14) may have developed in the older rats, thus limiting the vasodilator action o f urotensin I. The present observations o f different blood pressure levels in the male and female hypertensive rats (170.6 ± 2.3 and 145 ± 2.9 mm Hg, respectively) sup port a previous report o f similar differences in spontaneously hypertensive rats (13).…”

Section: Discussionsupporting

confidence: 78%

Pharmacological Effects of Urotensins

Medakovic

Lederis

1975

Pharmacology

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The blood pressure lowering effect of urotensin I, a vasodilatatory peptide obtained from urophyses of a bony fish species (Catostomus commersoni) was studied by tail plethysmography in conscious normotensive and in spontaneously hypertensive rats. Urotensin I (10 mU/100 g body weight i.v.) lowered the blood pressure, depending on the preinjection level. The lowering of pressure amounted to 12.4 ± 1.28 % of the preinjection level in normotensive rats, 17.9 ± 1.46 % in hypertensive females and to 28.9 ± 1.06 % in hypertensive males. The differences between the normotensive and each group of hypertensive animals were statistically significant (p < 0.05 to p < 0.001).The blood pressure-lowering effect of urotensin I was less pronounced in female hypertensive rats than in hypertensive males of the same age.No significant difference was found in the preinjection blood pressure level between the group of younger (169–176 days) and older (247–249 days) male hypertensive rats. However, the blood pressure in the younger rats was significantly more affected by urotensin I than that in the older rats (p < 0.05).

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Section: Discussionsupporting

confidence: 78%

Pharmacological Effects of Urotensins

Medakovic

Lederis

1975

Pharmacology

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“…However, these findings might also be explained by a diminished reuptake of released NE (de Champlain et al, 1966) or by a storage defect of vesicular NE (Krakoff et aI., 1967). Although the increase in blood pressure produced by exogenous NE is augmented in animals made hypertensive by DOCA-salt (Schmid et al, 1967), the increased blood pressure has been attributed to arteriolar wall thickening rather than to enhanced receptor sensitivity to the catecholamines (Massingham and Shevde, 1971;Berlin and Ziakas, 1972). Others have been unable to demonstrate augmented responses to administered NE in this form of hypertension (Mizogami et al, 1972).…”

Section: Introductionmentioning

confidence: 96%

6-Hydroxydopamine destruction of central adrenergic neurones prevents or reverses developing DOCA-salt hypertension in rats

Lamprecht¹,

Richardson²,

Williams³

et al. 1977

J. Neural Transmission

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The role of brain catecholaminergic neurones in the pathogenesis of DOCA-salt hypertension in the rat was investigated by selective depletion of central catecholamines using intraventricular or intracisternal administration of 6-hydroxydopamine (6-OHDA). Only the intraventricular injections prevented the development of hypertension. In addition, intraventricular 6-OHDA reversed the hypertension produced by two weeks but not six weeks of DOCA-salt treatment. The ability of intraventricular injections of 6-OHDA to prevent or reverse DOCA-salt hypertension while intracisternal injections do not, appears to be related to the greater depletion of brain catecholamines produced by the intraventricular injections. Only in the spinal cord and in the locus coeruleus were the norepinephrine contents depleted equally by either injection route. These findings suggest that central catecholaminergic neurones other than those originating in the locus coeruleus or descending in the spinal cord are important in the initiation, but not in the long term maintenance, of DOCA-salt hypertension. The influence of the central catecholamine neurons involved in the development of DOCA-salt hypertension might be mediated neurally via nonadrenergic pathways or hormonally via the brain-pituitary-endocrine system.

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“…The parent AS colony in Dunedin has a blood pressure under ether anaesthesia of about 145-150 mmHg (Heslop & Phelan, 1973) which was about the level existing in the main GH colony at that generation. However, a branch of the AS strain in England seems to have a higher blood pressure and has in fact been used for hypertension work (Massingham & Shevde, 1971).…”

mentioning

confidence: 99%

Studies on the New Zealand Strain of Genetically Hypertensive Rats

et al. 1973

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S U M M A R Y1. The New Zealand strain of rats with genetic hypertension (GH rats), the Japanese strain with spontaneous hypertension and the salt-sensitive strain of Dahl are now well established as three genetically pure lines for use in hypertensive research. Other pure lines not consciously selected for high blood pressure have also recently been shown to exhibit hypertension.2. In the GH rats the inheritance of the blood pressure appears to be polygenic; thus a simple causation of the hypertension appears unlikely. The inheritance is also complex in the other pure lines of hypertensive rats.3. In the GH rats variation in intake of sodium from 0.050/, to 1 0/, of the solid diet does not affect the development of the hypertension.4. The renin-angiotensin-aldosterone system does not appear to play a primary role in the initiation of the hypertension in the GH rats. Compared with normotensive rats of the parent colony, plasma and renal renin aredecreased, total exchangeableand carcass sodium are decreased, as are also the plasma volume and total extracellular fluid volume. Plasma sodium is normal and plasma potassium increased.5. There is no evidence of a primary abnormality of catecholamine storage or turnover. Prevention of the development of the sympathetic nervous system from birth does not entirely abolish the difference in blood pressure between GH rats and comparably treated normotensive rats.6. The increased peripheral resistance in blood-perfused hind limbs and tails of GH rats is due both to increased neurogenic and myogenic components and to a structural element. Increased vascular reactivity to a variety of constrictor agents is readily demonstrated in saline-perfused preparations.7. The different strains of hypertensive rats may in their diversity mirror the differences between the various forms of human essential hypertension. 15s 16sF. 0. Simpson et a/.

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Aortic reactivity and electro‐physiology in normotensive rats, spontaneously hypertensive rats and rats made hypertensive with desoxycorticosterone plus salt

Cited by 9 publications

References 2 publications

Pharmacological Effects of Urotensins

Pharmacological Effects of Urotensins

6-Hydroxydopamine destruction of central adrenergic neurones prevents or reverses developing DOCA-salt hypertension in rats

Studies on the New Zealand Strain of Genetically Hypertensive Rats

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