Effect of 6-Hydroxydopamine on Neonate Spontaneously Hypertensive and Normotensive Rats

1976 ◽  
Vol 17 (3) ◽  
pp. 419-419 ◽  
Author(s):  
Masayori OZAKI ◽  
Kazunobu SUGAWARA ◽  
Naoko TAKAMI ◽  
Masashi OGAWA ◽  
Masami NIWA
Keyword(s):  
Spontaneously Hypertensive ◽  
6 Hydroxydopamine

The relationship between altered blood vessel structure, hypertension, and the sympathetic nervous system

1985 ◽  
Vol 63 (4) ◽  
pp. 387-391 ◽  
Author(s):  
T. M. Scott ◽  
G. Galway
Keyword(s):  
Sympathetic Innervation ◽  
Diabetic Rats ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Sd Rat ◽  
Vessel Structure ◽  
Wistar Kyoto ◽  
Hypertension Development ◽  
6 Hydroxydopamine ◽  
The Relationship

The relationship between sympathetic innervation and arterial medial development has been examined in normotensive, hypertensive, and diabetic rats. Using the jejunal artery as a model, the number of nerve fibres innervating the artery as determined from fluorescent preparations, and the medial thickness and lumen diameter as measured from resin embedded specimens were correlated from animals prepared in various ways. The rats used were normal Sprague–Dawley (SD), SD with induced hypertension, SD with diabetes induced with streptozotocin, SD sympathectomized with 6-hydroxydopamine, spontaneously hypertensive rats (SHR), SHR treated with capsaicin to prevent hypertension development, Wistar Kyoto rats (WKY), and WKY treated with capsaicin. Examination of the jejunal arteries from these rats at 12 weeks of age following normal development, or 8 weeks of hypertension development, or 8 and 12 weeks of diabetes, showed that increased innervation occurred in the SHR under all conditions, and in the diabetic rats after 8 weeks of diabetes. Medial hypertrophy occurred in the SHR and in the SD hypertensive only. It is concluded that the special relationship which exists between the sympathetic innervation and arterial media in the SHR does not occur during hypertension development in the SD rat, nor is it necessary for normal medial development in the SD rat. The sympathetic innervation does appear to have a trophic influence on vascular smooth muscle of diabetic rats, at least in the early stages of the disease.

Catecholamines, Blood Pressure, Renin and Myocardial Function in the Spontaneously Hypertensive Rat

1976 ◽  
Vol 51 (s3) ◽  
pp. 455s-459s
Author(s):  
Suzanne Oparil ◽  
Lynda Erinoff ◽  
A. Cutilletta
Keyword(s):  
Blood Pressure ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Myocardial Function ◽  
Spontaneously Hypertensive Rat ◽  
Plasma Renin ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Spontaneously Hypertensive ◽  
6 Hydroxydopamine

1. Neither nerve-growth-factor antiserum (NGFAS) administered subcutaneously nor 6-hydroxydopamine administered intraventricularly to immature spontaneously hypertensive rats (SHR) inhibited the development of the hypertensive syndrome. In contrast, NGFAS did not affect blood pressure in normotensive Kyoto/Wistar rats. 2. Peripheral vascular resistance was increased and cardiac index decreased in both NGFAS and 6-hydroxydopamine-treated SHR despite preservation of normal blood pressure. 3. NGFAS treatment did not influence the development of left ventricular hypertrophy in SHR, despite the lowering of blood pressure. In contrast, 6-hydroxydopamine caused an attenuation in the development of left ventricular hypertrophy. 4. Indices of left ventricular contractility were depressed by NGFAS treatment but not by 6-hydroxydopamine. 5. Plasma renin activity was unaffected by NGFAS treatment and increased by 6-hydroxydopamine.

Mechanism of action of vasoconstrictor responses to atriopeptin II in conscious SHR

1985 ◽  
Vol 249 (6) ◽  
pp. R781-R786 ◽  
Author(s):  
R. W. Lappe ◽  
J. A. Todt ◽  
R. L. Wendt
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Sympathetic Nerves ◽  
Spontaneously Hypertensive ◽  
Regional Vascular Resistance ◽  
6 Hydroxydopamine ◽  
Renal Vascular ◽  
Renal Sympathetic

Previous studies have demonstrated that infusion of synthetic atriopeptin II (AP II) lowered arterial pressure, reduced regional blood flow, and increased total peripheral and regional vascular resistances in conscious spontaneously hypertensive rats (SHR). This study was designed to examine the mechanism(s) involved in regional vasoconstrictor responses to AP II. In these experiments, hemodynamic actions of AP II were examined in control, 6-hydroxydopamine-treated (chemically sympathectomized), and renal-denervated groups of instrumented conscious SHR. Infusion of AP II (1 microgram X kg-1 X min-1) caused similar reductions in mean arterial pressure in control (-22 +/- 2 mmHg), chemically sympathectomized (-23 +/- 2 mmHg), and renal-denervated (-23 +/- 3 mmHg) SHR. In control SHR, AP II infusion reduced renal (-20 +/- 3%), mesenteric (-26 +/- 2%), and hindquarters (-18 +/- 10%) blood flow and increased regional vascular resistance in all three beds. Chemical sympathectomy prevented the fall in renal blood flow (RBF) and significantly abolished the regional vasoconstrictor responses to AP II infusion. In unilateral renal-denervated groups of SHR, AP II reduced renal vascular resistance (RVR) -11 +/- 3% but failed to alter RBF (-3 +/- 1%) in denervated kidneys. In contrast, RVR increased (20 +/- 7%) and RBF was significantly reduced (-29 +/- 3%) in contralateral-innervated kidneys. This study demonstrated that chemical or surgical destruction of renal sympathetic nerves abolished AP II-induced increases in RVR. These data further indicate that in conscious SHR the regional vasoconstrictor responses to AP II infusion appear to be mediated by increases in sympathetic tone rather than through direct vascular actions of AP II.

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