Renal periarterial nerve stimulation-induced vasoconstriction at low frequencies is primarily due to release of a purinergic transmitter in the rat

D. D. Schwartz, Kafait Malik

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Abstract

In the isolated rat kidney, the vasoconstrictor response elicited by periarterial nerve stimulation at low frequencies (2 Hz) is resistant to alpha adrenergic receptor blockade. It has been proposed that in some blood vessels ATP is coreleased with norepinephrine during nerve stimulation to activate P2-purinergic receptors and is responsible for the component of the vasoconstrictor response that is resistant to alpha adrenergic receptor blockade. To assess the contribution of a purinergic transmitter in the vasoconstriction elicited by periarterial nerve stimulation in the isolated Tyrodes-perfused rat kidney, fractional overflow of [3H]norepinephrine and vasoconstrictor responses to renal nerve stimulation were examined after alpha adrenergic receptor blockade and/or P2-purinergic receptor desensitization. The alpha-1 adrenergic receptor antagonists prazosin (0.1-1.0 μM) and corynanthine (0.1-1.0 μM) and the nonselective alpha adrenergic receptor antagonist phentolamine (0.1-1.0 μM) did not significantly reduce vasoconstrictor responses elicited by low frequency (0.5-4 Hz) but attenuated the responses to high-frequency (6-10 Hz) periarterial nerve stimulation. At low-frequency renal nerve stimulation, selective p2-purinergic receptor desensitization abolished the vasoconstriction at 0.5 Hz and dramatically attenuated the responses up to 4 Hz. In the presence of prazosin, the component of the vasoconstrictor response that was resistant to alpha adrenergic receptor blockade at all frequencies of renal nerve stimulation was abolished after treatment with α,β-methylene ATP. On the other hand, in the isolated perfused rabbit kidney, prazosin (1.0 μM) alone reduced dramatically the vasoconstrictor responses to periarterial nerve stimulation over the same frequencies used in the rat. These data suggest that renal vasoconstriction elicited by periarterial nerve stimulation in the rat kidney is due primarily to release of a purinergic transmitter, probably ATP and, to a lesser extent, norepinephrine at low physiological frequencies of stimulation (< 4 HZ).

Original languageEnglish (US)
Pages (from-to)764-771
Number of pages8
JournalJournal of Pharmacology and Experimental Therapeutics
Volume250
Issue number3
StatePublished - 1989

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Vasoconstriction
Vasoconstrictor Agents
Receptors, Adrenergic, alpha
Kidney
Purinergic P2 Receptors
Prazosin
Norepinephrine
Adenosine Triphosphate
Adrenergic alpha-1 Receptor Antagonists
Adrenergic Antagonists
Yohimbine
Phentolamine
Blood Vessels
Rabbits

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

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title = "Renal periarterial nerve stimulation-induced vasoconstriction at low frequencies is primarily due to release of a purinergic transmitter in the rat",
abstract = "In the isolated rat kidney, the vasoconstrictor response elicited by periarterial nerve stimulation at low frequencies (2 Hz) is resistant to alpha adrenergic receptor blockade. It has been proposed that in some blood vessels ATP is coreleased with norepinephrine during nerve stimulation to activate P2-purinergic receptors and is responsible for the component of the vasoconstrictor response that is resistant to alpha adrenergic receptor blockade. To assess the contribution of a purinergic transmitter in the vasoconstriction elicited by periarterial nerve stimulation in the isolated Tyrodes-perfused rat kidney, fractional overflow of [3H]norepinephrine and vasoconstrictor responses to renal nerve stimulation were examined after alpha adrenergic receptor blockade and/or P2-purinergic receptor desensitization. The alpha-1 adrenergic receptor antagonists prazosin (0.1-1.0 μM) and corynanthine (0.1-1.0 μM) and the nonselective alpha adrenergic receptor antagonist phentolamine (0.1-1.0 μM) did not significantly reduce vasoconstrictor responses elicited by low frequency (0.5-4 Hz) but attenuated the responses to high-frequency (6-10 Hz) periarterial nerve stimulation. At low-frequency renal nerve stimulation, selective p2-purinergic receptor desensitization abolished the vasoconstriction at 0.5 Hz and dramatically attenuated the responses up to 4 Hz. In the presence of prazosin, the component of the vasoconstrictor response that was resistant to alpha adrenergic receptor blockade at all frequencies of renal nerve stimulation was abolished after treatment with α,β-methylene ATP. On the other hand, in the isolated perfused rabbit kidney, prazosin (1.0 μM) alone reduced dramatically the vasoconstrictor responses to periarterial nerve stimulation over the same frequencies used in the rat. These data suggest that renal vasoconstriction elicited by periarterial nerve stimulation in the rat kidney is due primarily to release of a purinergic transmitter, probably ATP and, to a lesser extent, norepinephrine at low physiological frequencies of stimulation (< 4 HZ).",
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T1 - Renal periarterial nerve stimulation-induced vasoconstriction at low frequencies is primarily due to release of a purinergic transmitter in the rat

AU - Schwartz, D. D.

AU - Malik, Kafait

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N2 - In the isolated rat kidney, the vasoconstrictor response elicited by periarterial nerve stimulation at low frequencies (2 Hz) is resistant to alpha adrenergic receptor blockade. It has been proposed that in some blood vessels ATP is coreleased with norepinephrine during nerve stimulation to activate P2-purinergic receptors and is responsible for the component of the vasoconstrictor response that is resistant to alpha adrenergic receptor blockade. To assess the contribution of a purinergic transmitter in the vasoconstriction elicited by periarterial nerve stimulation in the isolated Tyrodes-perfused rat kidney, fractional overflow of [3H]norepinephrine and vasoconstrictor responses to renal nerve stimulation were examined after alpha adrenergic receptor blockade and/or P2-purinergic receptor desensitization. The alpha-1 adrenergic receptor antagonists prazosin (0.1-1.0 μM) and corynanthine (0.1-1.0 μM) and the nonselective alpha adrenergic receptor antagonist phentolamine (0.1-1.0 μM) did not significantly reduce vasoconstrictor responses elicited by low frequency (0.5-4 Hz) but attenuated the responses to high-frequency (6-10 Hz) periarterial nerve stimulation. At low-frequency renal nerve stimulation, selective p2-purinergic receptor desensitization abolished the vasoconstriction at 0.5 Hz and dramatically attenuated the responses up to 4 Hz. In the presence of prazosin, the component of the vasoconstrictor response that was resistant to alpha adrenergic receptor blockade at all frequencies of renal nerve stimulation was abolished after treatment with α,β-methylene ATP. On the other hand, in the isolated perfused rabbit kidney, prazosin (1.0 μM) alone reduced dramatically the vasoconstrictor responses to periarterial nerve stimulation over the same frequencies used in the rat. These data suggest that renal vasoconstriction elicited by periarterial nerve stimulation in the rat kidney is due primarily to release of a purinergic transmitter, probably ATP and, to a lesser extent, norepinephrine at low physiological frequencies of stimulation (< 4 HZ).

AB - In the isolated rat kidney, the vasoconstrictor response elicited by periarterial nerve stimulation at low frequencies (2 Hz) is resistant to alpha adrenergic receptor blockade. It has been proposed that in some blood vessels ATP is coreleased with norepinephrine during nerve stimulation to activate P2-purinergic receptors and is responsible for the component of the vasoconstrictor response that is resistant to alpha adrenergic receptor blockade. To assess the contribution of a purinergic transmitter in the vasoconstriction elicited by periarterial nerve stimulation in the isolated Tyrodes-perfused rat kidney, fractional overflow of [3H]norepinephrine and vasoconstrictor responses to renal nerve stimulation were examined after alpha adrenergic receptor blockade and/or P2-purinergic receptor desensitization. The alpha-1 adrenergic receptor antagonists prazosin (0.1-1.0 μM) and corynanthine (0.1-1.0 μM) and the nonselective alpha adrenergic receptor antagonist phentolamine (0.1-1.0 μM) did not significantly reduce vasoconstrictor responses elicited by low frequency (0.5-4 Hz) but attenuated the responses to high-frequency (6-10 Hz) periarterial nerve stimulation. At low-frequency renal nerve stimulation, selective p2-purinergic receptor desensitization abolished the vasoconstriction at 0.5 Hz and dramatically attenuated the responses up to 4 Hz. In the presence of prazosin, the component of the vasoconstrictor response that was resistant to alpha adrenergic receptor blockade at all frequencies of renal nerve stimulation was abolished after treatment with α,β-methylene ATP. On the other hand, in the isolated perfused rabbit kidney, prazosin (1.0 μM) alone reduced dramatically the vasoconstrictor responses to periarterial nerve stimulation over the same frequencies used in the rat. These data suggest that renal vasoconstriction elicited by periarterial nerve stimulation in the rat kidney is due primarily to release of a purinergic transmitter, probably ATP and, to a lesser extent, norepinephrine at low physiological frequencies of stimulation (< 4 HZ).

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