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 subjects, six asthmatic patients with mild essential hypertension, were aged 48 to 63 years and each was being treated with theophylline. Five patients received 10 mg of enalapril daily for two weeks and one received 5 mg for four weeks. Their bronchial responses to inhaled methacholine were measured with a modification of the 3-Hz oscillation method before and after the enalapril treatment. The patients' mean blood pressures decreased significantly from 180.7/100.3 to 152.0/93.3 mmHg after treatment. No treatment-associated changes in the frequency of coughing, the number of asthmatic attacks, or use of antiasthmatic drugs were noted. The results of the bronchial provocation tests revealed no changes in bronchial sensitivity or reactivity during treatment. Serum substance P levels were 61.3 pg/ml before treatment and 60.2 pg/ml after treatment. It is concluded that therapeutic doses of enalapril did not exacerbate asthmatic attacks or increase bronchial hypersensitivity in these asthmatic, hypertensive patients.
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PMID:Bronchial responses to enalapril in asthmatic, hypertensive patients. 169 64

Peripheral administration of the neuropeptide Substance P (SP) in rhesus monkeys and baboons caused a long lasting decrease in blood pressure, accompanied by a gradual normalization function of stress-induced bioelectrical activity changes in brain structures, relevant for cardiovascular regulation (frontal cortex, ncl. raphe, locus coeruleus). In addition, SP was found to normalize the disturbed interaction of brain structures of both hemispheres. Use of SP as a putative agent to treat essential hypertension in humans needs further studies.
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PMID:Neurophysiological effects of substance P in primate hypertension models. Preliminary report. 170 73

In the present study, the contents of plasma substance P (SP) and noradrenaline (NA) and adrenaline (AD) in human normotensive subjects and patients with essential hypertension as well as Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) were measured. The results showed that: (1) The levels of plasma SP in both hypertensive subjects were lower than that in both normotensive subjects. (2) The concentration of plasma NA and AD were significantly higher in patients with essential hypertension than that in normotensive subjects. (3) The levels of plasma SP increased and the concentrations of NA and AD decreased after antihypertensive drug treatment. These results suggest that both plasma SP and catecholamines were involved in essential hypertensive pathogenesis.
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PMID:[The role of plasma substance P and catecholamines in hypertension]. 171 54

Calcitonin gene-related peptide (CGRP), produced by alternative processing of the primary transcript of the calcitonin gene, is a potent vasodilator. We have shown that dietary calcium deficiency accompanied by decreased serum ionized calcium significantly decreases the neuronal content of CGRP in laminae I and II of the dorsal horn of the spinal cord in the growing rat. The spontaneously hypertensive rat (SHR) is characterized by decreased serum ionized calcium levels and is thought to most closely resemble human essential hypertension. To determine if the neuronal content of CGRP is decreased in the SHR compared to the Wistar-Kyoto (WKY) parent strain, CGRP was localized immunocytochemically in the dorsal horn of the spinal cord. The density of immunocytochemical staining was quantitated by computer-assisted image processing of laminae I and II of the upper thoracic spinal cord of 12-14 week old male SHR (n = 4) and WKY (n = 4) normotensive, control rats. The SHR had significantly decreased neuronal CGRP content compared to the WKY rats (107 +/- 5 vs 121 +/- 6 arbitrary units, P less than 0.01). In contrast, the neuronal density of substance P (SP), which frequently co-exists with CGRP in this neuronal population, was not different between the two groups (SHR, 91 +/- 6 (n = 4) vs WKY, 88 +/- 3 arbitrary units (n = 4)).
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PMID:Decreased spinal cord content of calcitonin gene-related peptide in the spontaneously hypertensive rat. 172 95

Administration of 10 micrograms of substance P intrathecally to the spinal T9 level of the adult rat, anaesthetized with urethane, provoked an increase in free catecholamines in plasma taken from the inferior vena cava. Adrenaline levels at 1 min after administration were 154.8 +/- 10.8% (mean +/- SE; n = 11) of preadministration levels and noradrenaline levels were 153.5 +/- 11.8% of preadministration levels. Differences between the values of free catecholamines in animals given substance P vs those given vehicle only were statistically significant at 1 and 10 min postinjection, but not at 30 min. Administration of a substance P analogue with central antagonistic properties 15 min before substance P was given prevented expression of the effects of substance P. These results suggest that substance P may be an excitatory chemical mediator of synaptic transmission in spinal pathways controlling adrenal medullary output. Thus dysfunction of substance P mechanisms may underlie some animal models of hypertension and may be involved in some cases of essential hypertension in man as well as in autonomic dysfunction associated with some neurological entities.
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PMID:Substance P given intrathecally at the spinal T9 level increases adrenal output of adrenaline and noradrenaline in the rat. 241 Aug 14

Administration of 10 micrograms of substance P intrathecally at the spinal T9 level of the unanaesthetized and the anaesthetized rat provoked an increase in arterial pressure and an increase in heart rate. Both cardiovascular responses began within 1-2 min of administration, and the peak of each occurred at 4-10 min. In the anaesthetized rat, which gave rise to the bulk of the responses reported, peak arterial pressure was ca 20 mm Hg greater than pre-administration levels, and peak heart rate was greater by ca 50 beats per min. Similar administration of vehicle failed to alter either parameter. Arterial pressure and heart rate in substance P-treated rats were significantly different from those in vehicle-treated rats up to 15-20 min after administration. Pretreatment with the sympathetic ganglion blocker, hexamethonium (10 mg/kg, i.v.), prevented the responses to intrathecal administration of substance P. Pretreatment with [D-Pro2, D-Phe7, D-Trp9]-substance P, an analogue with antagonist properties in the central nervous system, blocked both responses to substance P but failed to alter similar responses provoked by intrathecal administration of angiotensin II. Pretreatment with vehicle had no effect on responses to substance P or to angiotensin II. The antagonist also had partial agonistic effects. Both arterial pressure and heart rate were transiently increased, but this effect was reversed within 6 min; in the case of heart rate, values returned to the pre-application level but arterial pressure fell to a ca 15 mm Hg below this level. These results demonstrate a pharmacologically specific excitatory effect of substance P on spinal mechanisms controlling sympathetic output to the vessels and the heart; this output can be either via the adrenal medullae or via nerve pathways to the vessels and the heart. Our results also support the possibility that dysfunction of substance P systems at the spinal level may underly some models of hypertension and may be involved in some cases of essential hypertension in man, as well as in autonomic dysfunction associated with some neurological disorders.
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PMID:Substance P given intrathecally at the spinal T9 level increases arterial pressure and heart rate in the rat. 243 74

Substance P (SP) plays an important role in central nervous and peripheral blood pressure regulation. Its effects include modulating influence on the adrenergic system and inhibition of stress-induced plasma noradrenaline increase in animal studies. In patients with essential hypertension (n = 45, WHO stages 1 and 2) the SP-like immunoreactivity (SPLIR) was found significantly (p less than 0.01) lower (1.36 +/- 0.23 pg/100 microliters) than in 24 normotensive subjects (4.54 +/- 0.72 pg/100 microliters). Furthermore, the influence of a mental stress test on SPLIR was investigated in patients with essential hypertension (n = 11, WHO stage 1) and compared with nine normotensive subjects. Whereas in normotensive subjects plasma SP increased under a standardized mental arithmetic test (4.03 +/- 0.48 to 4.74 +/- 0.56 pg/100 microliters), in hypertensive patients a decrease of SP from lower baseline levels (2.85 +/- 0.54 to 2.57 +/- 0.54 pg/100 microliters) was demonstrated. The significantly different changes of plasma SP in normotensive and hypertensive subjects under mental stress conditions had the opposite direction in comparison with the adrenergic reaction [higher and prolonged increase of plasma noradrenaline (NA) in the hypertensive group]. Under antihypertensive drug treatment with prazosin (4.5 mg/day, n = 10) or with captopril (450 mg/day, n = 10) an increase of plasma SP was registered. The results support the participation of SP in the pathogenesis of human hypertension and in therapeutic mechanisms. Lower plasma levels and decreased responsiveness of SP possibly represent the enhanced stress sensitivity in primary hypertension.
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PMID:Substance P in human essential hypertension. 245 74

Since substance P is a potent natriuretic, diuretic, and vasodilatory peptide, a radioimmunoassay for substance P was developed, and its levels measured in the plasma of normal subjects and patients with essential hypertension. The plasma substance P levels were 186+/-14 pg/ml in normal subjects and 164+/-3 pg/ml in hypertensive patients. When the sodium content of their diet was reduced to 10 mEq/day, substance P levels failed to change, but plasma renin activity and urinary kallikrein increased. An acute saline infusion also failed to alter plasma substance P levels. Assuming an upright posture increased plasma renin activity, but not substance P, in both groups of subjects. Thus, it appears that substance P is not involved in the control of blood pressure, kallikrein excretion or renin release in man.
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PMID:Plasma substance P levels in normotensive and hypertensive subjects. 616 96

Patients with essential hypertension (n = 45) had significantly lower substance P plasma levels (13.6 +/- 2.30 pg/ml) in comparison with a group of 24 normotensive subjects (45.4 +/- 7.18 pg/ml) analyzed by radioimmunoassay. Prazosin treatment for 2 weeks with 4.5 mg/day enhanced the substance P plasma level depending on its antihypertensive effect. Norepinephrine concentration in plasma was also elevated by prazosin. Dipeptidylpeptidase IV, dopamine-beta-hydroxylase and plasma renin activity were not changed significantly. The results indicate the participation of substance P in pathophysiological processes of human essential hypertension.
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PMID:Evidence of decreased plasma substance P levels in human essential hypertension and influence of prazosin treatment. 619 65

In this study, the concentration of plasma arginine vasopressin (AVP) and substance P (SP) in normotensive subjects as well as patients with essential hypertension was measured. The results showed that: (1) The concentration of plasma AVP in patients with essential hypertension (21.83 +/- 1.30ng/L) was significantly higher than that in normotensive subjects (11.02 +/- 1.05 ng/L) (P < 0.001). The level of plasma SP in hypertensive subjects (276.60 +/- 21.35 pmol/L) was obviously lower than that in normotensive subjects (958.20 +/- 31.13 pmol/L) (P < 0.001). (2) The level of plasma AVP decreased (from 24.88 +/- 1.63 to 8.69 +/- 1.39 ng/L, P < 0.001) and that of plasma SP increased (from 331.40 +/- 48.18 to 958.80 +/- 39.30 pmol/L, P < 0.001) after antihypertensive drug treatment. (3) A negative correlation was found between the level of plasma AVP and SP in patients with essential hypertension (r = -0.564, P < 0.001), but no correlation was found between them in normotensive subjects (r = -0.096, P > 0.05). It is suggested that the abnormal level of plasma AVP and SP plays a role in the pathogenesis of hypertension.
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PMID:[The role of arginine-vasopressin and substance P in the pathogenesis of hypertension and their interrelation]. 750 32


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