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PubMed1981

Inhibition of adrenergic neuroeffector transmission in rabbit pulmonary artery and aorta by adenosine and adenine nucleotides.

The effect of adenosine and adenine nucleotides on sympathetic neuroeffector transmission in the rabbit isolated pulmonary artery and aorta was studied. Adenosine (10(-5)-3 x 10(-4)M) decreased the contractile response of pulmonary artery and aorta evoked by electrical-field stimulation. The decrease was reversible. No tachyphylaxis developed. Inhibition of either adenosine deaminase by deoxycoformycin (3.6 x 10(-6)M) or of adenosine transport by dilazep (3 x 10(-6)M) did not alter the inhibitory effect of adenosine on the neurogenic contractions in the pulmonary artery. However, deoxycoformycin plus dilazep markedly enhanced the inhibitory effect of adenosine. The calcium antagonists nifedipine (1.5 x 10(-8)M) and nimodipine (1.3 x 10(-8)M) had no effect on the adenosine-induced inhibition. This was also the case with theophylline (5 x 10(-5)M), atropine (10(-7)M), and the prostaglandin synthetase inhibitors indomethacin (5 x 10(-5)M and suprofen (3 x 10(-5)M). The contractile response of the pulmonary artery elicited by exogenous (-)-noradrenaline (NA; 10(-9)-3 x 10(-4)M) was essentially not altered by adenosine (10(-5)-3 x 10(-4)M). Adenosine (10(-4)M) did not alter the spontaneous 3H-outflow from rabbit aorta preloaded with 3H-(-)-noradrenaline (3H-NA). Adenosine (10(-5)-3 x 10(-4)M), ADP (10(-4)M), ATP (10(-5)M), and inosine (10(-4)M) diminished the overflow of tritium from pulmonary artery and aorta preloaded with 3H-NA. The spontaneous outflow of tritium from aorta preloaded with 3H-NA consisted of 3H-NA (17%), 3H-dihydroxyphenylglycol (3H-DOPEG; 30%), 3H-dihydroxymandelic acid (3H-DOMA, 4%), 3H-O-methylated and deaminated metabolites (3H-OMDA; 42%), and 3H-normethanephrine (3H-NMN; 2%). Adenosine (10(-5) and 10(-4)M) enhanced 3H-DOPEG and 2H-NMN, decreased 3H-NA, and did not alter 3H-DOMA and 3H-OMDA. The stimulation-evoked overflow of tritium for aorta preloaded with 3H-NA consisted of 3H-NA (31%), 3H-DOPEG (18%), 3H-DOMA (2%), 3H-ONDA (46%), and 3H-NMN (3%). Adenosine (10(-5) and 10(-4)M) enhanced 3H-NA and 3H-DOPEG, decreased 3H-OMDA and did not alter 3H-DOMA and 3H-NMN. Adeosine (10(-6)-10(-4)M) did not alter the accumulation of 3H-NA (10(-8)M) by aorta. It is concluded that adenosine inhibits vascular sympathetic neuroeffector transmission by diminishing the release of transmitter from the nerve terminals.

Adenine Nucleotides↗
PubMed1981

Dual effect of the muscarinic agonist McN-A-343 on vascular neuroeffector transmission.

The site and mechanism of action of McN-A-343 (4-m-chlorophenylcarbamoyloxy)-2-butynyltrime-thylammonium chloride) on sympathetic neuroeffector transmission in the rabbit isolated pulmonary artery was studied. Low concentrations (10(-6) - 3 x 10(-5) M) of McN-A-343 and cocaine enhanced (up to 210 and 236%, respectively) the contractions evoked by electrical-field stimulation, while higher concentrations (10(-4) -3 x 10(-4)M) inhibited them. McN-A-343 (10(-4)M) caused an initial transitory potentiation (222% of control) of the stimulation-evoked contractions followed by an inhibition. In the presence of cocaine (3 x 10(-5)M), the potentiation caused by McN-A-343 was prolonged and the secondary inhibitory phase was thus abolished. Physostigmine (10(-5) - 10(-4)M), hexamethonium (10(-5) M), atropine (3 x 10(-7) M), suprofen (10(-5) M), and 4-aminopyridine did not alter the effect of McN-A-343 (1-(-4)M). Cocaine (3 x 10(-5)M) and (+)-amphetamine (10(-5) M) reversed the McN-A-343-evoked block, while they did not alter the inhibition caused by tetracaine (3.2 x 10(-5) M). Atropine (3 x 10(-7) M) had no effect on the McN-A-343-induced block, while 4-aminopyridine (10(-4) M) caused a partial and transitory reversal. On the aorta McN-A-343 (10(-4)M) did not alter the contractile concentration-response curve of (-)-noradrenaline (10(-9) - 3 x 10(-4)M), while that of serotonin (10(-8) - 3 x 10(-5)M) was moved to the right in a competitive manner. McN-A-343 (10(-4)M) did not alter the contractions evoked by noradrenaline (10(-7) M) during the period corresponding to the stimulation-evoked enhancement and subsequent inhibition. McN-A-343 (10(-4)M) slightly antagonized the contractions caused by tyramine (10(-6) - 10(-3) M) and carbachol (10(-6) - 10(-3) M). It is concluded that McN-A-343 enhances stimulation-evoked transmitter release by a presynaptic facilitatory action mediated via receptors localized on the outer surface of adrenergic neurones and to a lesser extent by inhibition of noradrenaline re-uptake. The enhancement does not involve presynaptic nicotine or muscarine receptors. Furthermore, McN-A-343 inhibits transmitter release by acting as an adrenergic neurone blocking agent at an intraneuronal site. The inhibition does not involve presynaptic muscarine inhibitory receptors and is prostaglandin-independent.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1987

Non-adrenergic, non-cholinergic parasympathetic secretion in the rat submaxillary and sublingual glands.

Atropine resistant secretion from the submaxillary and sublingual glands was demonstrated upon electrical stimulation of the chorda-lingual nerve at high frequencies. The flow rate of the protein-rich saliva was low, and it declined rapidly and markedly upon prolonged stimulation. The results show that one or more substances other than acetylcholine are released by parasympathetic stimulation and that they may be of importance for the regulation of the exocrine functions of the glands. When the continuous mode of electrical stimulation at a low frequency of the nerve was changed to an intermittent mode of stimulation at a high frequency (in the absence of atropine), the secretion of fluid and protein decreased.

Animals↗
PubMed1989

Effect of pinacidil on sympathetic neuroeffector transmission in rabbit blood vessels.

The effects of pinacidil on vascular sympathetic neuroeffector transmission were studied. Pinacidil (3 x 10(-7)-3 x 10(-4) M) inhibited the contractions of rabbit isolated pulmonary artery evoked by nerve stimulation. This was the case both in the absence and presence of cocaine plus corticosterone. The inhibition reached a steady state and was reversible. Pinacidil (10(-5) -3 x 10(-4) M), in the absence or presence of cocaine plus corticosterone, markedly enhanced the 3H-overflow evoked by electrical-field stimulation of the artery preloaded with 3H-noradrenaline (3H-NA). The enhancement was dependent on frequency (1-30 Hz) in a complex manner. Phentolamine (3 x 10(-6) M), but not rauwolscine (10(-6) M) prevented the enhancement. Pinacidil (10(-4) M) did not antagonize the alpha-methylnoradrenaline-induced inhibition of 3H-overflow evoked by stimulation. Pinacidil (10(-5)-3 x 10(-5) M) in a non-competitive manner antagonized the contractions of isolated aorta elicited by noradrenaline (3 x 10(-9)-3 x 10(-5) M), phenylephrine (2 x 10(-8)-3 x 10(-4) M), adrenaline (10(-9)-3 x 10(-5) M), histamine (10(-6) 6 x 10(-4) M), serotonin (10(-8)-10(-4)M), and potassium (10(-3) M). Pinacidil (10(-6)-3 x 10(-4) M) and methacholine (3 x 10(-8)-10(-6) M) relaxed aorta preconstricted with noradrenaline (10(-7) M). The relaxation caused by pinacidil was not dependent on the presence of endothelial cells, while that seen with methacholine was.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1978

Neuroeffector maturity of portal veins from newborn rats, rabbits, cats and guinea pigs.

Isolated portal veins from newborn and adult rats, rabbits, cats and guinea pigs were studied isometrically. Spontaneous activity and induced responses to transmural nerve stimulation (NS), noradrenaline, tyramine, acetylcholine and BaCl2 were quantitated. In agreement with our previous observations the portal veins of the newborn rat was found to lack spontaneous activity and responsiveness to applied stimuli whereas the newborn rabbit's portal vein showed inconsistent and weak responses. In the neonatal cat and guinea pig portal veins the pattern of the spontaneous activity and induced responses resembled those found in vessels from adult animals. It is concluded that the portal vein maturity at birth in several respects dramatic neuroeffector development of the portal vein during the postnatal period in the rat corresponds to prenatal events in cats and guinea pigs which are more highly developed at birth. Consequently, the lack of responsiveness of the portal vein during the first week of life does not seem to be secondary to the hormonal and hemodynamic adjustments during the neonatal period. Rather, the postnatal development of the rat portal vein occurs according to a genetically predetermined schedule, possible in parallel with the ontogenesis of vascular control in general.

Acetylcholine↗
PubMed1992

Neuro-effector characteristics of sweat glands in the human hand activated by irregular stimuli.

Intraneural electrical stimulation of cutaneous fascicles in the median nerve was performed in 24 normal subjects and the effects on sweating within the innervation zone were monitored as changes of skin resistance and water vapour partial pressure (wvpp). The aims were: (1) to investigate the response variability between repeated stimulation sequences in the same skin site and between different sites and (2) to compare quantitative effects of regular and irregular stimulation on skin resistance and wvpp. Regional axillary anaesthesia of the brachial plexus eliminated spontaneous and reflex sympathetic activity. With repeated irregular stimulation sequences skin resistance responses from the same skin site varied only slightly between trials. Differences between response curves from two skin sites in the same subject or from different subjects were also small but significantly greater (P < 0.01) than differences between responses to repeated stimulation in the same site. Irregular stimulation with average frequencies of 0.49 Hz and 3.51 Hz gave greater resistance responses than if the same number of stimuli were delivered regularly (P < 0.01). The difference was most pronounced at 0.49 Hz. At an average frequency of 0.49 Hz the stimulation usually evoked no changes of wvpp whereas an average frequency of 3.51 Hz caused an increase of wvpp which was greater with irregular than with regular stimulation in all subjects. We conclude that: (1) sweat responses to sudomotor nerve traffic vary slightly due to local factors in the skin or the terminal nerve endings and (2) irregular sudomotor nerve traffic evokes more sweat than if the same impulses occur regularly.

Adult↗
PubMed1994

Skin sympathetic nerve activity and effector function during sleep in humans.

Multi-unit sympathetic skin nerve activity (SSA) in the peroneal nerve was recorded together with electrical skin resistance, skin blood flow and (in some subjects) finger blood pressure during sleep in 22 sleep-deprived healthy subjects. The average strength of sympathetic activity in different sleep stages was measured during 5-min periods as the area-under-curve of the integrated neurogram. Stage 2 sleep was reached by 15 subjects, stages 3-4 by nine and rapid eye movement (REM) sleep by six subjects. Non-REM sleep was always associated with an increased skin resistance, which was larger in glabrous than in hairy skin (293 +/- 48 vs. 175 +/- 4% of awake control level, n = 10, P < 0.05). Skin blood flow also increased during sleep, with a mean maximal increase of 397 +/- 79% of the awake control level (n = 11, P < 0.05). In spite of these changes of effector function no significant difference in mean SSA was found between the awake control period and periods of non-REM sleep, but during REM sleep SSA increased with 34% (P < 0.05) compared with the immediately preceding stage 2 period. In stage 2 sleep, K-complexes were associated with bursts of SSA followed by transient changes of skin resistance, blood flow and arterial blood pressure. When both skin resistance and blood flow were recorded within the innervation area of the impaled fascicle, single bursts or short periods of increased SSA could be succeeded by increased skin blood flow without concomitant skin resistance change. This indicates the existence of specific sympathetic vasodilator fibres in the skin. Therefore the unchanged strength of multiunit SSA during non-REM sleep in the face of increases of skin resistance and blood flow may be a consequence of an increased sympathetic vasodilator nerve activity combined with decreases of vasoconstrictor and sudomotor traffic.

Adult↗
PubMed1990

Development of cholinergic neuroeffector transmission in the avian heart. Implications for regulatory mechanisms.

A brief outline of the ontogenesis of cholinergic neuroeffector transmission in the embryonic chick heart is given. It is important to define the development of neuroeffector transmission to evaluate the possible effects on postjunctional membrane properties. The membrane response of the aneural chick heart undergoes a qualitative change to muscarinic agonist at a time well before cholinergic innervation. This suppressed response can be revealed later in life, even in adults, when provision is made to exclude Gi/Go and or K channel activity.

Acetylcholine↗
PubMed1980

Facilitatory effect of nicotine on adrenergic neuroeffector transmission in the isolated ear artery of the rabbit.

The effects of nicotine were studied on perfusion pressure and vasoconstrictor responses to sympathetic nerve stimulation in the isolated ear artery of the rabbit. Infusions of nicotine (50 micro M) produced a transient increase in perfusion pressure and potentiated responses to nerve stimulation; these effects of nicotine were unaffected by atropine (0.3 micro M) and abolished or significantly reduced respectively by hexamethonium (300 micro M) or mecamylamine (1 micro M). In experiments with ear arteries previously labelled with [3H] noradrenaline an infusion of nicotine (50 micro M) produced a transient increase in tritium efflux and the potentiation of responses to nerve stimulation in the presence of nicotine was accompanied by a statistically significant increase in stimulation-induced tritium efflux; these effects of nicotine were abolished by hexamethonium (300 micro M) or mecamylamine (1 micro M).

Animals↗