Alterations in the field stimulation-induced release of endogenous norepinephrine from the coccygeal artery of spontaneously hypertensive and Wistar-Kyoto rats.

The field stimulation-induced release of endogenous NE from the isolated caudal artery from 5-6, 8-10 and 28-30 week old SHR resulted in a greater release of transmitter compared to age-matched WKY. The alpha 2-selective adrenoceptor antagonist, yohimbine produced a significant enhancement in the release of NE from both SHR and WKY of 5-6 and 10-12 and 28 week old WKY but release was attenuated in 28 week old SHR. It is concluded that the enhanced release of NE contributes to the development of hypertension in the SHR.

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.

Effect of low sodium diet on the facilitatory effect of angiotensin on 3H-norepinephrine release in the rat portal vein.

The ability of angiotensin to enhance the field-stimulation induced release of 3H-norepinephrine from the superfused rat portal vein was examined in vessels obtained from animals fed a normal (0.5% Na+) or low sodium diet (0.05% Na+). Angiotensin was seen to enhance the field-stimulation (480 pulses, 2 Hz, 1 ms duration, supramaximal voltage) induced release of 3H-norepinephrine from vessels obtained from Sprague-Dawley, Wistar, Wistar-Kyoto (WKY) and the spontaneously hypertensive rats (SHR) maintained on a normal sodium diet. The effect of angiotensin was attenuated when examined in vessels obtained from animals maintained on the low sodium diet. The selectivity of the low sodium diet for angiotensin was demonstrated by a lack of effect of the low sodium diet in altering the facilitatory effect of isoproterenol on the release of 3H-norepinephrine and an enhanced response to the alpha 2-adrenoceptor-selective antagonist, yohimbine. The simultaneous treatment of rats with a low sodium diet plus captopril (estimated to be approximately 50 mg/kg/day for 7 days) prevented the attenuation of the angiotensin-induced enhancement of the release of 3H-norepinephrine seen by sodium alone. These results are consistent with the hypothesis that low sodium treatment increases circulating angiotensin levels which lead to a down-regulation of the angiotensin receptors located on adrenergic nerve varicosities.

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.

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)