Action of angiotension on myocardial and renal catecholamines in the rabbit.
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Angiotensin II↗
Biomedical subjects
T C Westfall
Publications and source records attributed to T C Westfall.
Influence of aging on catecholamine levels, accumulation, and release in F-344 rats.
Neuronal function in selected brain areas has been evaluated in Fischer 344 rats aged 2-4 months, 11-14 months and 21-26 months. In vitro release of 3H-norepinephrine from hypothalamus and occipital cortex and 3H-dopamine from striatum has been evaluated using potassium, amphetamine, and field-stimulation. In vitro uptake of 3H-catecholamines has been evaluated in the same tissues. Catecholamine levels were measured in six brain areas: hypothalamus, striatum, cortex, cerebellum, brainstem and midbrain. Significant age-related decreases of NE levels, uptake, and release to high frequency stimulation were seen in the hypothalamus. The decreases in 3H-NE uptake and NE levels in the hypothalamus were apparent at 12 months, whereas the decrease in 3H-NE release after high frequency stimulation was seen in the senile rats.
Aging↗
Effect of sodium depletion on the release of [3H]norepinephrine from central and peripheral tissue of Wistar-Kyoto and spontaneously hypertensive rats.
To study the relationship between sodium intake, the sympathetic nervous system, and hypertension, we studied the effects of a 7-9 day dietary restriction of sodium in three different ages of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Field-stimulated [3H]norepinephrine ( [3H]NE) release was measured in portal vein, anterior hypothalamus, and the A2 region of the nucleus tractus solitarius (NTS) of 5- to 6-, 10- to 11-, and 28- to 30- week-old SHR and age-matched WKY. A low-sodium diet (0.05% Na+, control 0.5% Na+) significantly lowered stimulated [3H]NE release from portal vein and anterior hypothalamus in SHR and WKY at all three ages. However, release from the A2 region was not altered by sodium restriction. The results of the present study suggest that lowered dietary sodium can selectively alter norepinephrine release in both the peripheral and central sympathetic nervous system of SHR and WKY. The results also suggest that the SHR at 5-6 weeks are more sensitive to altered dietary sodium than are age-matched WKY.
Animals↗
Enhancement of methacholine-stimulated guanosine 3':5'-cyclic monophosphate formation in supersensitive guinea pig vasa deferentia.
Decentralization of the guinea pig vas deferens resulted in supersensitivity of the contractile response to methacholine. Methacholine also elevated cyclic GMP to a greater extent in the decentralized vas deferens than in sham-operated controls. Decentralization did not alter basal cyclic AMP or cyclic GMP content. These observations are analogous to the enhanced responsiveness of cyclic AMP formation in supersensitive beta adrenergic systems.
Animals↗
Angiotensin facilitation of 3H-norepinephrine release in central tissue of spontaneously hypertensive rats but not in Wistar-Kyoto rats: effects of sodium depletion.
The purpose of the present study was to determine the ability of angiotensin II to facilitate the field stimulation-induced release of 3H-norepinephrine from brain areas of three ages of normal or salt-restricted spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Angiotensin II facilitated the stimulation-induced release of 3H-norepinephrine from the anterior hypothalamus of 5-6, 10-11, and 28-30 week-old SHR but not age-matched WKY. Angiotensin II failed to alter 3H-norepinephrine release in the A2 region of the nucleus tractus solitarius of either SHR or WKY, at all ages tested. Placement of rats on a sodium-restricted diet for 7 days abolished the facilitation of induced 3H-norepinephrine release by angiotensin, seen in the SHR at 5-6 and 10-11 weeks, but not that at 28-30 weeks. These results suggest that angiotensin II can facilitate noradrenergic release in the anterior hypothalamus of SHR but not WKY. This facilitation by angiotensin II in SHR can be altered by placement of the rats (5-6, 10-11 week-old) on a sodium-restricted diet.
Aging↗
Angiotensin facilitation of noradrenergic neurotransmission in central tissues of the rat: effects of sodium restriction.
This study investigated the ability of angiotensin II (Ang II) to facilitate the stimulation-induced release of [3H]norepinephrine [( 3H]NE) from two cardiovascular regulatory areas in normal and sodium-restricted rats. Ang II (10(-7) M) facilitated the field-stimulation-induced release of [3H]NE from the A2 area of the nucleus tractus solitarius but not from the anterior hypothalamus of Sprague-Dawley and Wistar rats. Placement of rats on a sodium-restricted diet abolished the facilitation of [3H]NE release due to Ang II. Captopril given during sodium restriction partially restored the facilitory effects of Ang II. In an effort to determine the interaction of Ang II and sodium reduction, the effects of chronic Ang II were studied. Seven-day intravenous Ang II infusions blocked the facilitory effect of Ang II on [3H]NE release in a manner similar to that seen with sodium restriction. These results suggest that low sodium diets may alter the facilitation of [3H]NE release by Ang II by interactions with the renin-angiotensin system.
Angiotensin II↗
Noradrenergic transmission in the isolated portal vein of the spontaneously hypertensive rat.
The effect of electrical field stimulation (1, 2, 5, 10 Hz for a total of 480 pulses at 15-minute intervals) on the release of 3H-norepinephrine from the superfused portal vein of spontaneously hypertensive rats (SHR) or Wistar-Kyoto rats (WKY) of various ages was studied. The ages of the animals were (in weeks) 5-6 (prehypertensive), 8-10 (young hypertensives), 16-18 (older hypertensives), and 28 (mature hypertensives). There was no difference in the release of 3H-norepinephrine or developed tension of the portal vein to any frequency of field stimulation of SHR or WKY at 5-6 weeks of age. However, there was a significantly greater release of 3H-norepinephrine and developed tension of veins of SHR in response to low (1 or 2 Hz) but not high frequencies (5 or 10 Hz) at 8-10, 16-18, and 28 weeks of age. Vessels from hypertensive animals also developed greater resting tension and spontaneous activity, which was reduced to that of WKY in the presence of an alpha-adrenergic antagonist. The alpha 2 selective adrenergic antagonist yohimbine produced the same degree of enhancement of release of 3H-norepinephrine to field stimulation of veins obtained from both SHR and WKY at 5-6, 8-10 and 16-18 weeks of age. However, the facilitory effect of yohimbine was significantly attenuated in portal veins obtained from SHR at 28 weeks of age compared to age-matched WKY.(ABSTRACT TRUNCATED AT 250 WORDS)
Age Factors↗