Drugs online research references
Eur J Pharmacol. 1985 Feb 26;109(2):289-92.
Neuropeptide Y (NPY): enhancement of blood pressure increase upon alpha-adrenoceptor activation and direct pressor effects in pithed rats.
Dahlof C, Dahlof P, Lundberg JM.
The effects of neuropeptide Y (NPY) on blood pressure and heart rate were studied in pithed rats. Systemic infusion of NPY in a dose (230 pmol X kg-1 X min-1) which per se did not affect blood pressure enhanced the pressor response to phenylephrine (50 nmol X kg-1 i.v.) and that to electrical stimulation of the sympathetic outflow. In higher doses, NPY caused a pressor effect per se, which was dose-dependently antagonized by nifedipine but not by adrenoceptor antagonists. In conclusion, NPY enhanced the alpha-adrenoceptor-mediated response and had Ca2+-dependent vasoconstrictor activity in vivo.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2987001&dopt=Abstract
Circulation. 1998 Mar 10;97(9):865-70.
Arginine vasopressin enhances sympathetic constriction through the V1 vasopressin receptor in human saphenous vein.
Medina P, Acuna A, Martinez-Leon JB, Otero E, Vila JM, Aldasoro M, Lluch S.
Department of Physiology, University of Valencia, Spain.
BACKGROUND: Arginine vasopressin (AVP) not only acts directly on blood vessels through V1 receptor stimulation but also may modulate adrenergic-mediated responses in animal experiments in vivo and in vitro. The aim of the present study was to investigate whether AVP can contribute to an abnormal adrenergic constrictor response of human saphenous veins. METHODS AND RESULTS: Saphenous vein rings were obtained from 32 patients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension. AVP (3x10[-9] mol/L) enhanced the contractions elicited by electrical field stimulation at 1, 2, and 4 Hz (by 80%, 70%, and 60%, respectively) and produced a leftward shift of the concentration-response curve to norepinephrine (half-maximal effective concentration decreased from 6.87x10[-7] to 1.04x10[-7] mol/L; P<.05). The V1 vasopressin receptor antagonist d(CH2)5Tyr(Me)AVP (10[-6] mol/L) prevented the potentiation evoked by AVP. The selective V1 receptor agonist [Phe,2 Orn8]-vasotocin (3x[-10]-9 mol/L) induced potentiation of electrical stimulation-evoked responses, which was also inhibited in the presence of the V1 receptor antagonist (10[-6] mol/L). In contrast, the V2 receptor agonist desmopressin (10[-9] to 10[-7] mol/L) did not modify neurogenic responses, and the V2 receptor antagonist [d(CH2)5, D-Ile,2 Ile,4 Arg8]-vasopressin (10[-8] to 10[-6] mol/L) did not prevent the potentiation induced by AVP. The dihydropyridine calcium antagonist nifedipine (10[-6] mol/L) did not affect the potentiating effect of AVP. CONCLUSIONS: The results suggest that low concentrations of AVP facilitate sympathetic neurotransmission and potentiate constrictor effects of norepinephrine in human saphenous veins. These effects appear to be mediated by V1 receptor stimulation and are independent of calcium entry through dihydropyridine calcium channels. Thus, AVP may contribute to vascular mechanisms involved in acute ischemic syndromes associated with venous grafts, particularly if the sympathetic nervous system is activated.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9580082&dopt=Abstract
Biochem Biophys Res Commun. 1992 Oct 15;188(1):440-5.
P-glycoprotein possesses a 1,4-dihydropyridine-selective drug acceptor site which is alloserically coupled to a vinca-alkaloid-selective binding site.
Ferry DR, Russell MA, Cullen MH.
Department of Pharmacology, University of Birmingham, The Medical School, Edgbaston, United Kingdom.
[3H]Vinblastine bound with high affinity to surface membranes prepared from H69/LX4 cells which express P-glycoprotein (P-gp) and as a consequence are multidrug resistant (MDR). The KD was 9.8 +/- 1.5 nM and density of sites 31.2 +/- 8.6 pmol/mg of protein. [3H]Vinblastine binding was inhibited by cytotoxics and agents known to reverse MDR. 1,4-Dihydropyridine MDR reversing agents including nicardipine and nifedipine accelerated the dissociation of [3H]vinblastine from P-gp indicating a negative heterotropic allosteric effect. Cyclosporin A, vincristine and actinomycin D did not alter [3H]vinblastine dissociation kinetics. It is concluded that P-gp possesses at least two allosterically coupled drug acceptor sites, receptor site-1 that is selective for vinca alkaloids and cyclosporin A, and receptor site-2 that is selective for 1,4-dihydropyridines.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1358068&dopt=Abstract
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