Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of the present study was to investigate the effects of vasoactive neuropeptides, such as substance P or neurotensin, on vascular adrenergic neurotransmission in hypertension. In perfused mesenteric vasculatures prepared from spontaneously hypertensive rats (SHR), we examined the effects of substance P and neurotensin on vascular responsiveness and noradrenaline release from the sympathetic nerve endings. Stimulation-evoked noradrenaline release and pressor responses were inhibited by substance P and neurotensin. In SHR, the noradrenaline release and pressor responses during electrical nerve stimulation were significantly greater than in Wistar-Kyoto rats (WKY). The inhibitory effects of these responses by substance P and neurotensin were attenuated in SHR compared with WKY. These results showed that substance P and neurotensin could affect the presynaptic site of the blood vessels and cause a decrease in electrically stimulated noradrenaline release from the vascular adrenergic neurons. The reduction of noradrenaline release and pressor responses by substance P and neurotensin in SHR might suggest insufficient regulation of the vascular adrenergic transmission by these vasoactive peptides in hypertension.
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PMID:Role of substance P and neurotensin in the regulation of neurosecretion and vascular responsiveness in hypertension. 246 74

Unilateral removal of the afferent fibers of the IXth and Xth cranial nerve (nodose ganglionectomy) caused significant decrease in the content of substance P-like immunoreactivity (SP-LI) and neurokinin A-like immunoreactivity (NKA-LI) in the nucleus tractus solitarii (NTS) of rats. Microinjection of SP (1 ng) or NKA (10-100 ng) into the NTS caused prompt, transient hypotension and bradycardia, suggesting that SP and NKA may be neurotransmitters of the baroreceptor reflex in the NTS. NKB-like immunoreactivity (NKB-LI) was also detected in the NTS of rats by radioimmunoassay, but its content in the NTS was not affected by unilateral nodose ganglionectomy. The microinjection of 1-10 ng of suc-[Asp5, Me-Phe8]-SP(6-11) (senktide, a selective neurokinin B receptor peptide) into the NTS caused long-lasting hypertension and tachycardia. These results indicate that NKB may also be a neuromodulator on cardiovascular responses in the NTS.
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PMID:Cardiovascular roles of tachykinin peptides in the nucleus tractus solitarii of rats. 247 79

In 13 anaesthetized hens in the peak phase of their first laying year the influence of intravenously injected substance P (SP), 1-10 micrograms/animal, on oviductal pressure, duodenal pressure, blood pressure and heart rate has been studied within 5 h of oviposition. The neuropeptide induced a significant pressure increase in the different segments of the oviduct (infundibulum, magnum, isthmus, uterus and vagina) as well as in the duodenum. Blood pressure revealed a distinct biphasic response: a short period of hypotension accompanied by a tachycardia and a more pronounced and sustained hypertension, inducing a subsequent bradycardia. The complexity of the observed effects demonstrates the overall impact of intravenously administered SP on the anaesthetized hen.
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PMID:The influence of substance P on oviductal, duodenal and blood pressure in the anaesthetized domestic hen. 247 85

Substance P-like immunoreactivity (SPI) was investigated in the superior cervical ganglion of normotensive and genetically hypertensive (GH) Otago Wistar rats aged 1, 2, 8-10 and 50-60 weeks, by used of an indirect immunoperoxidase method. SPI was not seen in neuronal cell bodies but a subpopulation of ganglion cells was supplied by SP-positive terminals which closely invested the cell surface. This subpopulation showed no particular topographical distribution. The number of SP-positive terminal varicosities per unit area was several times higher in GH rats than in normotensive rats at all ages over 2-60 weeks. The proportion of neurons supplied by SP-positive terminals (sampled in 8-10 week-old rats) was also greater in GH than in normotensive rats. Decentralization of the ganglion or chronic capsaicin treatment removed all SP-immunoreactive terminals around the cell bodies, indicating that the SP-positive terminals are collaterals of thoracic sensory afferents. As SP has been reported to have an excitatory effect in sympathetic ganglia, intraganglionic release of SP might contribute to the development of hypertension in the GH strain.
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PMID:Substance P immunoreactivity in the superior cervical ganglia of normotensive and genetically hypertensive rats. 247 36

Little is known of the significance of perivascular peptides in hypertension. In this study we have investigated the circulating levels of calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) and substance P- like immunoreactivity (SP-LI) during and after treatment of severe hypertension. Seventeen patients with a mean blood pressure of 204/127 mmHg were included. Circulating levels of CGRP-LI and SP-LI in normotensive controls were 35 +/- 4 and 1.2 +/- 0.1 pmol/l, respectively. In the hypertensives CGRP-LI was significantly lower (22 +/- 3 pmol/l: P less than 0.05) while SP-LI did not differ (1.6 +/- 0.3 pmol/l) from the normotensives. After treatment the circulating level of CGRP-LI was still significantly lower (16 +/- 2 pmol/l: P less than 0.001) while SP-LI remained unchanged when compared with the controls. These observations suggest an involvement of vascular afferent nerves in the aetiology of hypertension in man.
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PMID:Reduced levels of calcitonin gene-related peptide (CGRP) but not substance P during and after treatment of severe hypertension in man. 247 45

Perivascular innervation of the mesenteric arteries of 7-week-old and 6-month-old spontaneously hypertensive rats and normotensive Wistar-Kyoto rats was examined. The densities of neuropeptide Y-containing nerve fibers and adrenergic nerve fibers were increased in the distal regions of mesenteric arteries of spontaneously hypertensive rats as compared with findings in Wistar-Kyoto rats. However, the densities of cholinergic nerve fibers, vasoactive intestinal polypeptide-containing, and substance P-containing nerve fibers in the mesenteric arteries of the spontaneously hypertensive rats were unchanged in comparison with findings in the Wistar-Kyoto rats. Thus, not only adrenergic nerve fibers but also neuropeptide Y-containing nerve fibers may play an important role in the development and maintenance of hypertension in spontaneously hypertensive rats.
Hypertension 1989 Dec
PMID:Perivascular innervation of the mesenteric artery in spontaneously hypertensive rats. 247 2

Intrathecal administration of VIP to the thoracic spinal cord in the urethane anaesthetized rat provoked a dose-dependent increase in heart rate without any change in arterial pressure. The cardioacceleration observed following administration of 6.5 nmol of VIP at the T9 level (n = 8) occurred within 1-2 min of administration, with a peak effect of 70-85 bpm, 10-30 min after administration. The magnitude of the maximum change when this dose was given at the T2 level (n = 8) was approximately 100 beats per min, 7-8 min after administration. However, the differences between T2 and T9 administration were not statistically significant. Intravenous administration of 6.5 nmol of VIP (n = 6) mimicked the cardioacceleratory effect of intrathecal administration, and also decreased systolic and diastolic arterial pressure by 9-13 mmHg 6-13 min after administration. The cardioacceleration observed following intrathecal administration at T9 was not blocked by prior systemic administration of the autonomic ganglion blocker hexamethonium (5 mg/kg) or by bilateral vagotomy. Nor was the effect blocked by prior intrathecal administration of the local anaesthetic lidocaine (250 micrograms), although lidocaine did block the tachycardia and hypertension resulting from intrathecal administration of substance P. Considered collectively, the findings that the cardioacceleration observed following intrathecal VIP injection is mimicked by i.v. administration, is not reversed by blockade of nicotinic transmission of autonomic ganglia or by bilateral vagotomy, and is not blocked by lidocaine suggest that VIP's tachycardic effect does not result from a direct action on spinal mechanisms mediating autonomic control of the cardiovascular system, but occurs via diffusion to a site of action outside the central nervous system.
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PMID:Cardioacceleration provoked by intrathecal administration of vasoactive intestinal peptide (VIP): mediation by a non-central nervous system mechanism. 248 50

Little is known about perivascular neuropeptides in hypertension in man. In this study we investigated the circulating levels of calcitonin gene-related peptide (CGRP)-, substance P- and vasoactive intestinal peptide-like immunoreactivity in 30 patients with severe hypertension before and after treatment for high blood pressure. Circulating levels of CGRP- and substance P-like immunoreactivity in the hypertensives were significantly different from the corresponding levels in 31 age- and sex-matched normotensive subjects. After normalization of blood pressure the mean levels of CGRP- and substance P-like immunoreactivity did not differ between the two groups. The levels of vasoactive intestinal peptide-like immunoreactivity remained unchanged. These observations suggest that vascular afferent nerves play a part in the maintenance of hypertension.
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PMID:Circulating perivascular dilatory neuropeptides in hypertension. 248 31

The occurrence and distribution of peptide-containing nerve fibers to the cerebral circulation are described. Immunocytochemical studies have revealed that cerebral blood vessels are invested with nerve fibers containing neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), peptide histidine isoleucine (PHI), substance P (SP), neurokinin A (NKA), and calcitonin gene-related peptide (CGRP). In addition, there are studies reporting the occurrence of putative neurotransmitters such as cholecystokinin, dynorphin B, galanin, gastrin releasing peptide, vasopressin, neurotensin, and somatostatin. The nerves occur as a longitudinally oriented network around large cerebral arteries. There is often a richer supply of nerve fibers around arteries than veins. The origin of these nerve fibers has been studied by retrograde tracing and denervation experiments. These techniques, in combination with immunocytochemistry, have revealed a rather extensive innervation pattern. Several ganglia, such as the superior cervical ganglion, the sphenopalatine ganglion, the otic ganglion, and small local ganglia at the base of the skull, contribute to the innervation. Sensory fibers seem to derive from the trigeminal ganglion, the jugular-nodose ganglionic complex, and from dorsal root ganglia at level C2. The noradrenergic and most of the NPY fibers derive from the superior cervical ganglion. A minor population of the NPY-containing fibers contains VIP instead of NA and emanates from the sphenopalatine ganglion. The cholinergic and the VIP-containing fibers derive from the sphenopalatine ganglion, the otic ganglion, and from small local ganglia at the base of the skull. Most of the SP-, NKA-, and CGRP-containing fibers derive from the trigeminal ganglion. Minor contributions may emanate from the jugular-nodose ganglionic complex and from the spinal dorsal root ganglia. NPY is a potent vasoconstrictor in vitro and in situ. VIP, PHI, SP, NKA, and CGRP act via different mechanisms to induce cerebrovascular dilatation. The sympathetic, the parasympathetic, and the sensory systems appear to be involved in modulating cerebrovascular tone in hypertension and in conditions of threatening vasoconstriction, e.g., subarachnoid hemorrhage and migraine.
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PMID:Neuropeptides in the cerebral circulation. 270 77

A large number and variety of compounds (acetylcholine, adenosine diphosphate, adenosine triphosphate, arachidonic acid, bradykinin, Ca2+ ionophores, calcitonin gene-related peptide, histamine, hydralazine, substance P, thrombin, and vasoactive intestinal polypeptide) have been shown to relax arterial smooth muscle indirectly. The endothelium in muscular arteries from several species appears to have receptors for these vasodilators. Binding of one of these compounds to its endothelial receptors results in the release (and presumably synthesis) of substance(s) that act on arterial smooth muscle to cause relaxation. The name endothelium-derived relaxing factor (EDRF) has been proposed for the substance or substances responsible for inhibition of contraction. Studies to determine additivity of endothelium-dependent relaxing agents and sensitivity of EDRF-mediated responses to a variety of inhibitors suggest that a single factor or a single common mechanism induces relaxation of vascular smooth muscle. Pharmacological studies have been equivocal with regard to the postulated involvement of phospholipases or arachidonic acid and to the suggestion that EDRF is an oxidative, non-cyclooxygenase product of arachidonate. Experiments on transfer of EDRF and reversal of endothelium-dependent relaxation consistently indicate that EDRF is quite labile. There is convincing evidence that EDRF activates smooth muscle guanylate cyclase, which results in an increase in intracellular cyclic guanosine 3',5'-monophosphate levels. The stimulation of guanylate cyclase by EDRF provides a valuable and sensitive parameter for studies with arteries as well as cells in culture. At present, the identity of EDRF and its role in cardiovascular homeostasis are unknown.
Hypertension
PMID:Endothelium-derived vascular relaxing factor. 298 29


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