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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. In the perfused rat mesenteric vascular bed, the effects of angiotensin II, cortisol and prostaglandin E2 on the vascular responses to noradrenaline or potassium chloride were studied. 2. Angiotensin II in subpressor concentrations potentiated the vasoconstrictor response to noradrenaline and potassium chloride. This effect of angiotensin II was inhibited in the presence of indomethacin and prostaglandin E2. 3. Cortisol in physiological concentrations inhibited the potentiating effect of angiotensin II. 4. Prostaglandin E2 enhanced the vasoconstrictor response to noradrenaline. This effect was not abolished by cortisol. 5. These results suggest that some actions of angiotensin II and cortisol in vivo are mediated by the regulation of prostaglandin synthesis or release.
Clin Sci Mol Med 1977 Sep
PMID:Potentiation of pressor effects of noradrenaline and potassium ions in the rat mesenteric arteries by physiological concentrations of angiotensin II: effects of prostaglandin E2 and cortisol. 91 46

1. The initial blood pressure response to saralasin (Sar1-Ala8-angiotensin II) infusion was examined in 15 normal subjects, eight patients with untreated essential hypertension and 65 patients established on chronic haemogialysis (including six anephric patients), and related to measurements of plasma renin activity (PRA), angiotensin II, plasma catecholamines (noradrenaline and adrenaline), blood volume and extracellular fluid volume ([35S]sulphate space or exchangeable sodium). 2. A transient rise in arterial pressure, maximum after 5-6 min, occurred in all normal subjects, patient with essential hypertension and anephric patients, and in 41 of the 59 dialysis patients with kidneys. 3. In the normal subjects, saralasin infusion resulted in a significant rise in plasma noradrenaline (mean increase 360%, P less than 0-02) without change in plasma adrenaline concentration. The change in noradrenaline was significantly related to the change in mean blood pressure (P less than 0-05) and was similar to the response to 5 min of a 40 degree head-up tilt. 4. An increase in plasma noradrenaline also occurred in dialysis patients (P less than 0-005) but the change in mean blood pressure with saralasin in this group was inversely related to PRA (P less than 0-001) and angiotensin II (P less than 0-001), directly related to blood volume (P less than 0-001), but unrelated to the change in plasma noradrenaline. 5. The pressor response to saralasin may be mediated not only by angiotensin-like action on vascular receptors but also by an action on the central or peripheral autonomic nervous system.
Clin Sci Mol Med 1977 Oct
PMID:Plasma catecholamines and the pressor response to Sar1-Ala8-angiotensin II in man. 91 58

Study is presented of the effect of noradrenaline on thermic denaturation of DNA-total histone complexes within the range of protein concentrations which corresponds to c1/c2 0-1.7 in solutions of 10(-3) M Na+ ionic strength (c1 and c2 being the weight concentrations of protein and nucleic acid, respectively). Denaturation of these systems has been found to be strongly affected by bivalent metals contained in DNA samples. Their presence accounts for the high temperature and wide melting range of DNA and diminution of the latter with an increase of the protein concentration in DNA-histone complexes. The denaturation parametres obtained for the studied systems are in fair agreement with predictions from the clip thermodynamic theory. Noradrenaline is shown to be capable of destabilizing DNA-total histon complexes. This is due to the inactivation of bivalent metals bound with DNA by noradrenaline. It is also suggested that noradrenaline does not weaken the histone binding with a nucleic acid.
Mol Biol (Mosk)
PMID:[Melting of DNA-total histone complexes in the presence of noradrenaline]. 105 66

1. The blood-bathed organ technique was used to study the release of catecholamines, angiotensin II and prostaglandin-like (PL) substances into the circulation during hypercapnia and after haemorrhage in anaesthetized dogs. 2. Elevated blood concentrations of noradrenaline, angiotensin II and prostaglandin-like substances have been detected during both experimental conditions. 3. The rise of arterial blood pressure during hypercapnia and after haemorrhage was associated with elevated concentrations of angiotensin II in the blood and could be abolished by inhibition of the angiotensin I-converting enzyme with SQ 20881. 4. The compensation of arterial pressure during both stresses was significantly impaired by release of prostaglandin-like substances; it could be restored by inhibition of prostaglandin biosynthesis with indomethacin. 5. The results indicate that activation of the renin-angiotensin system represents the major humoral mechanism for the maintenance of arterial pressure during hypercapnic acidosis and after haemorrhage.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Humoral response and blood pressure regulation during hypercapnia and haemorrhage in dogs. 107 98

1. Patients with mild essential hypertension and elevated plasma renin activity, when compared with normal subjects and hypertensive subjects with normal plasma renin, demonstrated features of sympathetic nervous cardiovascular excitation, accompanied by a raised plasma noradrenaline concentration. 2. An elevated heart rate at rest, shortened cardiac pre-ejection period, and greater heart rate reduction with acute beta-adrenoreceptor blockade (intravenous propranolol) in high-renin essential hypertension were indicative of adrenergic cardiac excitation. An elevated total of peripheral vascular resistance at rest and a greater fall in peripheral resistance with alpha-adrenoreceptor blockade (intravenous phentolamine) suggested the existence of a neurogenic increase in arteriolar resistance. 3. Blood pressure was normalized by 'total' autonomic blockade (atropine plus propranolol plus phentolamine) in the hypertensive subjects with elevated plasma renin activity. 4. These findings suggest that in mild high-renin essential hypertension increased adrenergic drive to the heart and resistance vessels exists. The elevation of blood pressure is sustained predominantly by neurogenic mechanisms. The high plasma renin activity is seen as an expression of sympathetic nervous system overactivity.
Clin Sci Mol Med Suppl 1976 Dec
PMID:High-renin essential hypertension: adrenergic cardiovascular correlates. 107 2

1. The addition of frusemide or bumetanide to perfusion fluid inhibited the response of the isolated mesenteric vascular bed to noradrenaline. 2. Addition of prostaglandin E2 to the perfusion fluid completely restored the response to noradrenaline. 3. Inhibition of prostaglandin secretion by indomethacin with restoration of responses to noradrenaline by the addition of exogenous prostaglandin E2 prevented the inhibitory effect of frusemide or bumetanide on responses to noradrenaline. 4. The inhibitory effects of diuretics on responsiveness to noradrenaline is mediated by blockade of endogenous prostaglandin synthesis.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Vascular actions of frusemide and bumetanide on the rat superior mesenteric vascular bed: interactions with prostaglandins. 107 22

1. Studies were made of the effects on responses to vasoconstrictor agents of prostaglandins released from Krebs perfused isolated kidneys of genetic hypertensive and normotensive rats. 2. Prostaglandin E-like activity, detected by bioassay, was released from kidneys of both groups of rats during the vasoconstriction produced by noradrenaline, angiotensin or prostaglandin F2alpha. 3. In preparations obtained from hypertensive rats, responses to higher doses of noradrenaline or angiotensin were initially greater than those from normotensive rats and these were then reduced to a greater extent by infusion of indomethacin, which abolished release of prostaglandin E-like activity. Thereafter, in kidneys of either group, vasoconstriction to noradrenaline was potentiated by infusion of prostaglandin E2. 4. We conclude that, in rats, renal prostaglandins released in response to vasoconstrictor agents could augment the effect of such agents and in genetic hypertensive rats release of renal prostaglandins could contribute to the disease.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Contribution of prostaglandins to the renal vascular supersensitivity to vasoconstrictor agents exhibited by New Zealand genetic hypertensive rats. 107 26

1. Deoxycorticosterone acetate (DOCA) implantation (100 mg/kg) caused mean arterial pressure to rise in 5-10 days from control pressures of 100-115 mmHg to stable hypertensive values of 140-160 mmHg in approximately 1 month. In six of seven pigs elevations of mean arterial pressure were entirely the result of increased total peripheral resistance. 2. Single implants maintained serum DOCA at approximately ten times normal concentration for up to 90 days. 3. Moderate but variable decreases in serum aldosterone followed implantation. 4. Hypokalaemia, polydipsia and suppressed plasma renin activity were evident by the fifth post-implantation day and persisted thereafter. No consistent change occurred in serum sodium. 5. Noradrenaline or angiotensin caused increases in total peripheral resistance at lower threshold infusion rates in hypertensive pigs compared with control animals. 6. In isolated, perfused hind-limb preparations, hypertensive vascular beds were characterized by both functional (increased vascular smooth muscle sensitivity) and structural (elevated resistance of maximally dilated vascular bed) changes. 'Protection' from increased arterial wall stresses in hypertensive pigs prevented structural, but not functional, alterations.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Deoxycorticosterone hypertension in the pig. 107 31

1. In chloralose-anaesthetized cats the centrally induced hypotensive effect of clonidine, and in some cases alpha-methyldopa, was diminished by pretreatment with a variety of tricyclic antidepressants and neuroleptic agents. 2. The interaction is assumed to occur at the central alpha-adrenoreceptors. Clonidine or alpha-methyl-noradrenaline (from alpha-methyldopa) are the agonists, and the aforementioned psychotropic drugs are the antagonists. 3. Psychotropic drugs which are not alpha-receptor blockers, like butyrophenone neuroleptics (pimozide and haloperidol) or benzodiazepine tranquillizers, do not significantly diminsh the centrally induced hypotensive effect of clonidine.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Reduction of the hypotensive effect of clonidine and alpha-methyldopa by various psychotropic drugs. 107 57

1. The pathogenesis of hypertension in spontaneously hypertensive rats (SHR) is considered to consist of neurogenic and non-neurogenic factors, both of which contribute to initiation and maintenance mechanisms. 2. Neurogenic factors have been demonstrated by the destruction of the central nervous system, sympathectomy, recording of sympathetic discharge, hind-limb perfusion and study of noradrenaline. These factors are mainly involved in the initiation of hypertension, and they appear to diminish in importance after the establishment of hypertension, as indicated by the noradrenaline-turnover study. 3. The non-neurogenic factors have been demonstrated haemodynamically by increased peripheral vascular resistance remaining even after sympathectomy. They have also been demonstrated histologically by the narrowing of resistance arteries with medial hyperplasia or hypertrophy. These factors appear to participate in maintenance mechanisms. 4. Increased incorporation of labelled amino acid into non-collagenous and collagenous protein of the arterial walls precedes medial hypertrophy and hyertensive arteriosclerosis. It seems to play a role therefore both during neurogenic initiation and later non-neurogenic maintenance of blood pressure. 5. Non-collagenous protein metabolism of arterial walls is increased in young SHR, and it is partly dependent on neural innervation as detected by surgical or pharmacological sympathectomy. It indicates a close linkage between neurological and structural changes in the initiation of spontaneous hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Neural and non-neural mechanisms in spontaneous hypertension. 107 58


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