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Biomedical subjects

C Su

Publications and source records attributed to C Su.

At least 145 records · Page 8Linked to original sources
PubMed1986

Influence of basal perfusion pressure on vasoconstrictor and vasodilator responses induced sympathetically and reflexly in pump-perfused rat hindquarters.

The hindquarters of Wistar rats, under pentobarbital anesthesia, were vascularly isolated and perfused at a constant flow rate (6.25 ml/min) with autologous blood. Basal perfusion pressure varied from 60 to 140 mm Hg during the experimental procedure and among individual rats. The magnitude of the constrictor effect of i.a. norepinephrine was virtually constant and independent of the basal pressure. I.A. injection of acetylcholine and histamine; i.v. injection of norepinephrine; and stimulation of the lumbar sympathetic nerves with pulses of 0.03 msec or less, produced dilator responses in the perfused extremities. Stimulation with pulses of 0.1 msec or more resulted in a constrictor response followed by a dilator response. These dilator responses increased linearly and the constrictor responses decreased linearly as the basal pressure increased. Thus, the law of initial value of resistance held true for all dilator responses tested and for the constrictor responses evoked by stimulation of the lumbar sympathetic nerves. This result permitted normalization of these responses to predicted values at a reference perfusion pressure (100 mm Hg) by statistical analysis. The dilator response elicited by stimulation with shorter pulses and the constrictor response elicited by longer pulses had the same time course, which suggests that the constrictor response is probably compounded by a synchronous dilator mechanism. Hexamethonium, guanethidine and prazocin abolished the dilator responses elicited by neural stimulation and those induced by i.v. norepinephrine. These results indicate that the responsiveness of pump-perfused rat hindquarters varies with the existing perfusion pressure in a linear fashion according to the law of initial value of resistance except in the case of i.a. norepinephrine. Both the electrically- and reflexly-evoked dilator responses require intact ganglionic and alpha-adrenergic transmission.

Acetylcholine↗
PubMed1985

Endothelium removal augments vasodilation by sodium nitroprusside and sodium nitrite.

Sodium nitroprusside (3-100 nM) and sodium nitrite (0.03-1 mM) caused relaxation of the rat aortic ring segments precontracted by norepinephrine. The relaxation was significantly augmented by removal of endothelium, and this augmentation was greater in the aorta from spontaneously hypertensive rats (SHR) than Wistar Kyoto rats (WKY). The mechanism remains unknown but such augmentation may be clinically favorable to the use of nitrovasodilators.

Adenosine↗
PubMed1984

Excitatory and inhibitory effects of 5-hydroxytryptamine in mesenteric arteries of spontaneously hypertensive rats.

Some of the presynaptic and postsynaptic excitatory and inhibitory actions of 5-hydroxytryptamine (5-HT) in the rat mesenteric arteries were reexamined with particular reference to the genetic hypertensive rat model. Mesenteric arteries were perfused and the perfusion pressure monitored in the presence or absence of 5-HT, norepinephrine or periarterial sympathetic nerve stimulation. The vasoconstrictor response to 5-HT was resistant to prazosin but effectively inhibited by cyproheptadine and ketanserin. The vasoconstrictor responses to norepinephrine and nerve stimulation were markedly potentiated by 5-HT, and this potentiation was blocked by ketanserin at concentrations which inhibited the 5-HT-induced vasoconstriction, while much higher concentrations were required for cyproheptadine. No significant difference was found in these regards between mesenteric arteries from the spontaneously hypertensive rats (SHR) and those from the normotensive Kyoto Wistar rats (WKY). 5-HT significantly increased the nerve stimulation-evoked 3H overflow in [3H]norepinephrine-treated mesenteric arteries of SHR, but reduced the 3H overflow in the WKY preparations. These results suggest that ketanserin-sensitive 5-HT2 receptors are involved in the potentiating effect of 5-HT in the rat mesenteric arteries, and that an increase in transmitter release by 5-HT may contribute to its potentiation of nerve stimulation-induced vasoconstriction in SHR.

Animals↗
PubMed1984

Potentiation by quipazine of adrenergic transmission in mesenteric arteries of spontaneously hypertensive rats.

The effect of quipazine on vasoconstrictor responses to periarterial sympathetic nerve stimulation (NS: 8 Hz, 2 ms, 30 s) and to exogenous norepinephrine (NE) were investigated in the isolated perfused mesenteric arteries of the spontaneously hypertensive rats (SHR) and the normotensive Wistar Kyoto rats (WKY). Quipazine (100 nM) potentiated the pressor response to NS significantly more than that to NE in both SHR and WKY. This agent (30 and 100 nM) also significantly increased the NS-evoked 3H overflow in the [3H]NE pretreated mesenteric vasculature of SHR, but not of WKY, suggesting facilitation of transmitter release. The summation of the pre- and postsynaptic effects of quipazine may account for its greater amplifying effects on NS in SHR, while this agent may act mainly postsynaptically in WKY. The presynaptic action is not attributable to alpha-adrenoceptor blockade but probably to a serotonin-like agonistic action, and the postsynaptic action appears to be mediated by ketanserin-sensitive (5HT2) receptors.

Animals↗
PubMed1984

Alpha-adrenoceptor- and prostaglandin-mediated modulation of vascular adrenergic neurotransmission in spontaneously hypertensive rats.

The modulation of vascular adrenergic neurotransmission in the spontaneously hypertensive rat (SHR) and Wistar-Kyoto rat (WKY) mediated by alpha-adrenoceptor and prostaglandin E2 (PGE2) were evaluated. The pressor responses of the perfused mesenteric vascular bed to perivascular adrenergic nerve stimulation (NS) and infusion of norepinephrine (NE) and the NS-induced 3H-efflux in preparations pretreated with 3H-norepinephrine were determined. In both SHR and WKY, a selective alpha 2 agonist, B-HT 920 (30-300 nM), inhibited neurogenic vasoconstriction, and B-HT 920 (100-300 nM) potentiated the pressor response to NE in a dose-dependent manner. The effects of B-HT 920 did not significantly differ in SHR and WKY. Another alpha 2 agonist, clonidine (100 nM), decreased the 3H-efflux approximately by 30% both in SHR and WKY. A selective alpha 2 blocking agent, yohimbine (3-300 nM), potentiated the neurogenic vasoconstriction and inhibited the pressor response to NE equally in SHR and WKY. No difference in enhancement of 3H-efflux by yohimbine (30-300 nM) was seen between SHR and WKY either in the absence or presence of cocaine (10 microM) and metanephrine (20 microM). PGE2 (0.1-1 microM) potentiated pressor responses to NS and NE in SHR and WKY, but this compound (1 microM) did not affect the NS-induced 3H-efflux in either group of rats. It appears that adrenergic neurotransmission is inhibited presynaptically via an alpha 2 receptor mechanism and facilitated postsynaptically by PGE2 in the rat mesenteric vascular bed. The hypertensive state in SHR can not be accounted for by alteration of these modulator mechanisms.

Animals↗
PubMed1984

Involvement of the vascular renin-angiotensin system in beta adrenergic receptor-mediated facilitation of vascular neurotransmission in spontaneously hypertensive rats.

This study was conducted to investigate the possible involvement of the vascular renin-angiotensin system in the isoproterenol (ISO)-induced facilitation of adrenergic neurotransmission in the mesenteric vasculature. The isolated, perfused mesenteric vascular beds from normotensive Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were used for these studies. ISO at concentrations from 10(-9) to 10(-6) M caused significantly greater enhancement of the pressor response to periarterial nerve stimulation (PNS) in preparations from SHR than in those from WKY. The pressor responses to exogenous norepinephrine (NE) were, however, inhibited by ISO to a similar degree in preparations from both WKY and SHR. The enhancement of the PNS response produced by ISO was markedly attenuated by propranolol at 5 X 10(-7) M (nonselective beta receptor blocker) and by ICI 118,551 at 5 X 10(-7) M (selective beta-2 receptor blocker), whereas practolol at 5 X 10(-6) M (selective beta-1 receptor blocker) caused a potentiation of the ISO-induced enhancement of responses to PNS in preparations from both WKY and SHR. All three beta blockers generally abolished the ISO-induced inhibition of the pressor responses to exogenous NE. The selective beta-2 adrenergic receptor agonists, salbutamol (3 X 10(-8) to 3 X 10(-7) M) and terbutaline (10(-7) to 3 X 10(-7) M), caused significantly greater enhancement of the PNS response in preparations from SHR than in those from WKY, whereas the selective beta-1 agonist, dobutamine, caused only inhibition of the PNS responses in preparations from both WKY and SHR. These three agonists all tended to reduce the pressor responses to exogenous NE. The ISO-induced enhancement of the responses to PNS was also significantly reduced by either captopril (5 X 10(-6) M) or [Sar1-Ile8]angiotensin II (5 X 10(-7) M) in preparations from SHR. Neither captopril nor [Sar1-lle8] angiotensin II had an effect on the pressor response to NE infusion or on the ISO-induced inhibition of NE responses. Angiotensin I produced an enhancement of the pressor responses to PNS and to NE infusion with the effect being greater on the response to PNS than to NE in the preparations from SHR but not in those from WKY. This enhancement of the PNS response by angiotensin I was abolished by either captopril (5 X 10(-7) M) or [Sar1-Ile8]angiotensin II (5 X 10(-7) M) in preparations from both WKY and SHR.(ABSTRACT TRUNCATED AT 400 WORDS)

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1983

Effects of adenosine on [3H]norepinephrine release from perfused mesenteric arteries of SHR and renal hypertensive rats.

Adenosine (10-30 microM) inhibited the 3H-efflux evoked by sympathetic nerve stimulation in the perfused rat mesenteric arteries preincubated with [3H]norepinephrine. The inhibition was smaller in the prehypertensive (5 weeks old) as well as hypertensive (15-18 weeks) SHR (spontaneously hypertensive rats), compared with age-matched normotensive Wistar Kyoto rats. However, it was not diminished in Wistar rats rendered hypertensive by left renal artery occlusion. Thus, a diminished adenosine-mediated presynaptic inhibition of adrenergic transmission appears to be genetically inherent in SHR.

Adenosine↗
PubMed1983

Purinergic neurotransmission and neuromodulation.

Conflicting views abound on the peripheral neurotransmitter and neuromodulator roles of purine compounds. Substantial organ- and species-related variations have become apparent. There is, however, a body of compelling evidence for such roles, if not so broad and ubiquitous as those envisioned (7) for the central nervous system. The variations may in part be attributable to the neuroeffector synaptic geometry. The transmitter concentration found at the postsynaptic membrane drops precipitously with increase in the synaptic cleft (85). Where the cleft is narrow, a purine may serve as the primary or sole transmitter (purinergic nerve) and presynaptic modulator. Alternatively, from nonpurinergic (e.g. adrenergic) nerves a purine may be released, possibly ATP by exocytosis, to act as a cotransmitter. It may also serve as pre- and post-synaptic modulator, potentially with a contribution from postsynaptic release (Figure 1). The purine could conceivably diffuse and affect other varicosities. Where the cleft is wide, the postsynaptic concentration of the neurogenic purine may be too low to permit a transmitter or postsynaptic modulator function. The concentration of the nonpurine transmitter may also be insufficient to elicit a significant postsynaptic purine release. The neuronally released purine may, however, presynaptically exert inhibition of transmitter release much as in a narrow cleft. It seems, therefore, that the origin of synaptic purines and their function, be it transmitter, cotransmitter, or modulator, are dictated at least in part by the characteristics of the purine pools, purinergic receptors, and synaptic configuration, which await further assessment.

Adenosine↗
PubMed1983

Effects of serotonin and some other neurohumoral agents on adrenergic neurotransmission in spontaneously hypertensive rat vasculature.

The effects of serotonin (5HT), acetylcholine (ACh), histamine and dopamine on the pressor responses of the mesenteric vasculature were examined in view of their potential role in neuromodulation. The responses to periarterial sympathetic nerve stimulation (NS, 8 Hz, 2 msec, 30 sec) and to exogenous norepinephrine (NE, 0.2 nmol) were compared between spontaneously hypertensive rats (SHR) and the control Wistar Kyoto rats (WKY). In both WKY and SHR, ACh (3-30 nM), histamine (0.3-3 microM) and dopamine (0.3 microM) attenuated the NS-induced vasoconstrictor response as much as the NE-induced response, indicative of predominance of postsynaptic inhibition. 5HT (10-100 nM) potentiated the vasoconstrictor responses to NS significantly less than that to NE in WKY, suggestive of presynaptic inhibition. Such difference was absent in SHR. These results suggest that the presynaptic inhibition of vascular adrenergic neurotransmission by 5HT is diminished in SHR, and this may contribute to the elevated blood pressure.

Acetylcholine↗
PubMed1982

Possible selective inhibition of [3H]adenosine uptake by papaverine in vascular adrenergic nerves.

The effect of the adenosine uptake inhibitors dipyridamole, papaverine and diazepam on the [3H]adenosine uptake was assessed using the rabbit pulmonary arterial segment. [3H]Adenosine uptake into the vascular segment was significantly diminished by dipyridamole (10(-6) -10(-5) M), papaverine (10(-5) -10(-4) M) or diazepam (5 x 10(-5) M) with potencies: dipyridamole greater than papaverine greater than diazepam. Dipyridamole (10(-6) M) or diazepam (5 x 10(-5) M) added 30 min before the incubation with [3H]adenosine reduced the high KCl-induced and epinephrine-induced [3H]purine effluxes equally, whereas papaverine (10(-5) M) selectively diminished the former efflux. KCl and epinephrine have been shown to act preferentially on the neuronal and extraneuronal sites, respectively. These results suggest that papaverine inhibits adenosine uptake into the vascular neuronal compartment, in preference to that into the extraneuronal compartment.

Adenosine↗
PubMed1982

Release of purines and noradrenaline by ouabain and potassium chloride from vascular adrenergic nerves.

1 Release of [3H]-noradrenaline and 3H-purine by ouabain (10(-4)M) or high KCl (50 mM) was investigated in the superfused rabbit pulmonary arterial segment preincubated with [3H]-noradrenaline or [3H]-adenosine. 2 Ouabain elicited a delayed large contraction and a parallel [3H]-noradrenaline efflux. These were substantially inhibited by Ca2+-free medium or preincubation with 6-hydroxydopamine (30 micrograms/ml, 30 min). 3 Ouabain caused an 3H-purine efflux which was slower than the [3H]-noradrenaline efflux. This was inhibited by 6-hydroxydopamine and in part by phentolamine (3 X 10(-6)M), indicating both neuronal and extraneuronal origins of purines. 4 In contrast to ouabain, high KCl appeared to induce predominantly purine efflux, which was phentolamine-insensitive and 6-hydroxydopamine-sensitive, indicative of neuronal origin. 5 It is suggested that the purine efflux evoked by ouabain and high KCl may originate from different neuronal vesicles.

Animals↗
PubMed1982

Enhanced angiotensin-mediated facilitation of adrenergic neurotransmission in spontaneously hypertensive rats.

The effect of angiotensin II on the pressor response of the mesenteric vascular bed to periarterial adrenergic nerve stimulation (PNS) was compared between spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). Angiotensin II (1-20 ng/ml) caused a marked potentiation of the vasoconstrictor response to PNS (8 Hz, 2 msec, for 30 sec) in a concentration-dependent manner without significantly affecting the base-line perfusion pressure in either WKY or SHR. The facilitatory effect of angiotensin II was significantly greater in SHR than in WKY preparations. The effective concentration for the peptide in SHR was approximately one-third of that found in WKY. Angiotensin II also potentiated the pressor response to exogenously administered norepinephrine (NE, 50 ng) in both WKY and SHR. The degree of potentiation of the response to PNS was greater than that to NE in SHR, while this differential was found only at high concentrations of angiotensin II on the WKY. The facilitatory effect of angiotensin II on the pressor response to either PNS or NE was markedly reduced by [Sar1-Ile8]angiotensin II (200 ng/ml) in both WKY and SHR. Angiotensin II caused further potentiation of the vasoconstrictor response to PNS or NE infusion in the presence of cocaine (5 micrograms/ml), which was of a greater magnitude in SHR than in WKY. These results suggest that the presynaptic facilitatory modulation of adrenergic vascular neurotransmission, mediated by angiotensin II receptors, is enhanced in the perfused mesenteric vascular bed of SHR.

Angiotensin II↗
PubMed1982

Augmentation by theophylline of [3H]purine release from vascular adrenergic nerves: evidence for presynaptic autoinhibition.

The effect of theophylline (a P1-purinoceptor blocker) on the tritium release evoked by high KCl (50 mM) and l-epinephrine (3 microM) was evaluated using [3H]adenosine-prelabeled pulmonary artery of the rabbit. It has previously been shown that KCl elicits purine release from adrenergic nerve terminals whereas epinephrine releases it from postsynaptic sites in this artery. The KCl-induced [3H]purine efflux was significantly enhanced by theophylline (10-100 microM), whereas the efflux induced by epinephrine (3 microM) was not enhanced but reduced by this drug at 100 microM. In contrast to theophylline, 1 to 3 microM adenosine or ATP significantly suppressed the KCl-induced purine efflux. This depolarization-induced efflux was not augmented by 10 microM papaverine or 3 microM phentolamine. Uptake of [3H]adenosine into the pulmonary arterial segment was strongly inhibited by 10 microM dipyridamole or papaverine, but not by the same concentration of theophylline. These findings suggest that the presynaptic autoinhibition mechanism may be involved in the purine release from vascular adrenergic nerves.

Adenosine↗
PubMed1982

Effect of superior cervical ganglionectomy on the sensitivity of rabbit ear artery and cerebral arteries of rabbit and cat to vasoactive agents.

The effect of sympathetic denervation on the sensitivity of the rabbit ear and basilar arteries and the cat middle cerebral artery to vasoactive agents was examined in relation to the functional significance of the innervation. Fourteen days after superior cervical ganglionectomy, the catecholamine fluorescence disappeared and the norepinephrine content drastically decreased and transmural nerve stimulation ceased to elicit any response in all these arteries. In the rabbit ear artery, denervation resulted in a significant leftward shift of dose-response curves for norepinephrine (8.2-fold), serotonin (7.7-fold), histamine (2.9-fold) and potassium (1.2-fold). In contrast, there was no significant shift of dose-response curves to these drugs in the rabbit basilar and cat middle cerebral arteries. These results indicate that after chronic superior cervical ganglionectomy, postjunctional supersensitivity developed in the rabbit ear artery, but no pre- or postjunctional supersensitivity occurred in the rabbit basilar and cat middle cerebral arteries. The difference may be in part attributable to the reported closer synaptic cleft distance of the sympathetic nerve terminals in the ear than in the cerebral arteries examined. These results further suggest that the sympathetic adrenergic nerve exerts a tonic influence over the rabbit ear artery, but little or none in normal cerebral blood vessels.

Animals↗
PubMed1981

Facilitation by clonidine of purine release induced by high KCl from the rabbit pulmonary artery.

1 The effect of clonidine on the 3H-purine release evoked by KCl or (-)-adrenaline was assessed in the superfused helical strip of the rabbit pulmonary artery pretreated with [3H]-adenosine. 2 Clonidine (3 x 10(-5) M to 10(-4) M) significantly enhanced the 3H-purine efflux evoked by 50 mM KCl but not by 3 x 10(-6) M) (-)-adrenaline. 3 This facilitatory effect of clonidine on the KCl-induced purine release was unaltered by phentolamine 3 x 10(-6) M. It was absent in arterial segments denervated with 6-hydroxydopamine 30 microgram/ml. 4 A sustained contractile response was evoked by clonidine 3 x 10(-5) M without an increase in the 3H-purine efflux. This was significantly reduced by phentolamine 3 x 10(-6) M, but not by yohimbine 10(-5) M or by denervation with 6-hydroxydopamine. 5 The uptake of [3H]-adenosine into the segments was not inhibited by clonidine 3 x 10(-5) M. 6 It is suggested that the facilitation by clonidine of the KCl-induced purine release is due to prevention of presynaptic autoinhibition of purine release from adrenergic nerves, by an antiadenosine action of the drug.

Adenosine↗