Relationship between the sympathetic nervous system and vascular smooth muscle: A morphometric study of adult and juvenile spontaneously hypertensive rat/Wistar-Kyoto rat caudal artery

1990 ◽  
Vol 5 (3) ◽  
pp. 129-139 ◽  
Author(s):  
Violet Albert ◽  
Gordon R. Campbell
Keyword(s):  
Nervous System ◽  
Smooth Muscle ◽  
Sympathetic Nervous System ◽  
Spontaneously Hypertensive Rat ◽  
Morphometric Study ◽  
Spontaneously Hypertensive ◽  
Caudal Artery ◽  
Wistar Kyoto Rat ◽  
Sympathetic Nervous ◽  
Wistar Kyoto

Vascular neuroeffector mechanisms in hypertension

1989 ◽  
Vol 67 (9) ◽  
pp. 1146-1150 ◽  
Author(s):  
D. W. Cheung
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Spontaneously Hypertensive Rat ◽  
Atp Release ◽  
Feedback Regulation ◽  
Release Mechanism ◽  
Neural Regulation ◽  
Spontaneously Hypertensive ◽  
Sympathetic Nervous ◽  
Presynaptic Adrenoceptors

Recent studies of the peripheral sympathetic nervous system indicate the presence of other vasoactive transmitters in addition to noradrenaline. There is now evidence suggesting ATP to be a co-transmitter of noradrenaline mediating the excitatory junction potential and the phentolamine-resistant component of the vasopressor response. In hypertension, changes in the neural regulation at both pre- and post-synaptic levels have been observed. In the spontaneously hypertensive rat (SHR), abnormal feedback regulation through presynaptic adrenoceptors and increases in release and uptake by the perivascular nerves are well characterized. Whether similar changes in the ATP release mechanism occur in the SHR and other forms of hypertension remain to be determined. A more important role for ATP in the neural regulation of the SHR tail artery has been proposed. In future studies, the possible contribution of co-transmitters to the responses should be taken into consideration.Key words: hypertension, noradrenaline, ATP, sympathetic nervous system.

scholarly journals ELECTRICAL STIMULATION OF THE NUCLEUS LOCUS COERULEUS ACTIVAT-ING THE SYMPATHETIC NERVOUS SYSTEM IN CONSCIOUS SPONTANEOUSLY HYPERTENSIVE RAT

1987 ◽  
Vol 28 (4) ◽  
pp. 622-622
Author(s):  
Hiromi Mitsubayashi ◽  
Hiroshi Kawamura ◽  
Masahiro Maki ◽  
Hideaki Higashi ◽  
Kazuyoshi Tsukamoto ◽  
...  
Keyword(s):  
Nervous System ◽  
Electrical Stimulation ◽  
Sympathetic Nervous System ◽  
Locus Coeruleus ◽  
Spontaneously Hypertensive Rat ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Sympathetic Nervous ◽  
Stimulation Of

Neuronal control of the kidney: Contribution to hypertension

1992 ◽  
Vol 70 (5) ◽  
pp. 759-770 ◽  
Author(s):  
J. Michael Wyss ◽  
Suzanne Oparil ◽  
Wanida Sripairojthikoon
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Renal Denervation ◽  
Spontaneously Hypertensive Rat ◽  
Renal Nerves ◽  
Sodium Retention ◽  
Spontaneously Hypertensive ◽  
Afferent Nerves ◽  
Hypertensive Rat ◽  
Sympathetic Nervous

The renal nerves contribute to hypertension in experimental models of the disease, and appear to play a role in human hypertension. Several lines of evidence indicate that both in spontaneously hypertensive rats and in deoxycorticosterone acetate–NaCl rats, the full development of hypertension is dependent on renal efferent nerves and their induction of excess sodium retention. Renal sensory (afferent nerve) feedback to the central nervous system does not contribute to either of these forms of hypertension. In contrast, renovascular hypertension in rats and aortic coarctation hypertension in dogs are mediated, at least in part, by overactivity of renal afferent nerves and a resultant increase in systemic sympathetic nervous system activity. These forms of hypertension are not associated with sodium retention, and selective sensory denervation of renal afferent nerves by dorsal rhizotomy and total renal denervation result in similar reductions in hypertension. Surprisingly, the renal nerves do not contribute to dietary NaCl exacerbated hypertension in the spontaneously hypertensive rat, dietary NaCl-induced hypertension in the Dahl NaCl-sensitive rat, or the chronic hypertensive and nephrotoxic effects of cyclosporine A therapy in the rat, despite the finding that in all three forms of hypertension, overactivity of the sympathetic nervous system is prominent. Clinical studies indicate that the renal afferent and efferent nerves contribute to hypertension of different etiologies. Together these data point to the complex role that the renal nerves likely play in human essential hypertension.Key words: kidney, cyclosporine, spontaneously hypertensive rat, renal deafferentation, renal denervation.

Increased pressor responses to pressor agents in spontaneously hypertensive rats

1979 ◽  
Vol 57 (1) ◽  
pp. 59-64 ◽  
Author(s):  
T. Kubo
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Spontaneously Hypertensive Rats ◽  
Wistar Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Pressor Responses ◽  
Sympathetic Nervous ◽  
Wistar Kyoto

Pressor reactivity to a variety of pressor agents after partial ganglionic blockade induced with hexamethonium was investigated in intact, in spinalized, and in chemically sympathectomized, spontaneously hypertensive rats (SHR). Responses of unanaesthetized 6-month-old SHR to noradrenaline, phenylephrine, and angiotensin after hexamethonium administration (32 mg/kg) markedly exceeded those of unanaesthetized, age-matched normotensive Wistar–Kyoto rats (WKR). Responses of anaesthetized SHR to noradrenaline after hexamethonium administration (16 mg/kg) were also increased at the hypertensive stages but not at the prehypertensive stages, when compared with those of anaesthetized normotensive Wistar rats of respective ages. In spinalized and chemically sympathectomized preparations after hexamethonium administration (16 mg/kg), noradrenaline produced equal increases in blood pressure in 6-month-old SHR and WKR. It is suggested that the functional sympathetic nervous system is important for the hyperreactivity of intact SHR.

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.

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