摘要:

SUMMARY1. Radioligand binding and functional studies were undertaken to investigate the P1‐purinoceptors present in the separated myometrial layers and the endometrium of the guinea‐pig uterus.2. In preparations of endometrium‐denuded circular myometrium, the A2‐selective agonists (2‐p‐(2‐carboxyethyl)phenethylamino‐5'‐N‐ethylcarboxamido‐adenosine (CGS 21680, 100 μmol/L) andN‐ethylcarboxamido adenosine (NECA, 1–10 μmol/L) inhibited contractile responses to phenylephrine. In preparations of endometrium‐intact circular myometrium, NECA (10 μmol/L) enhanced responses to phenylephrine. NECA did not modulate the spontaneous contractions of longitudinal myometrium.3. Homogenate binding studies with circular myometrium, longitudinal myometrium and endometrium revealed saturable high affinity [3H]‐NECA binding sites. The mean maximal densities of binding sites (Bmax) were 2.08, 14.7 and 15.5 fmol/mg protein, and pKD(neg. log dissociation constant) values were 9.82, 9.19 and 7.44, respectively.4. (R‐) and (S‐) ‐N6‐(2‐phenylisopropyl)adenosine (R‐ and S‐PIA) both competed for two [3H]‐NECA binding sites in preparations of circular myometrium. CGS 21680 competed for two [3H]‐NECA binding sites in preparations of endometrium and longitudinal myometrium. All other agonist competition was for one site only. The rank orders of potency of high affinity binding were S‐PIA ≥ R‐PIA ≥ CGS 21680 (circular myometrium), R‐PIA ≥ CGS 21680 ≥ S‐PIA (longitudinal myometrium) and CGS 21680>>S‐PIA ≥ R‐PIA (endometrium).5. In preparations of circular myometrium, longitudinal myometrium and endometrium the selective A1‐purinoceptor antagonist, 1,3‐dipropyl‐8‐(2‐amino‐4‐chloro)‐phenylxanthine (PACPX), competed for two [3H]‐NECA binding sites, the non‐selective antagonist 3,7‐dimethyl‐1‐propargylxanthine (DMPX), competed for one site only.6. NECA increased cyclic adenosine monophosphate (CAMP) levels in preparations of both circular myometrium and endometrium.7. These results indicate that P1‐purinoceptors of the A2‐subtype mediate the inhibitory effects of adenosine analogues on the phenylephrine‐induced contractions of the circular myometrium of the guinea‐pig, this effect is modified by the presence of the endometrium. There is no evidence that the [3H]

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb01642.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1. The relationships of respiratory sinus arrhythmia (RS A) and respiratory changes in systolic blood pressure (SBP) to tidal volume (VT) and breathing frequency (BF), were quantified during voluntary control ofVTand BF in healthy subjects.2. Respiration was measured non‐invasively with a respiratory inductive plethysmograph, which was calibrated prior to each study while breathing through a pneumotachygraph. Finger arterial blood pressure was measured non‐invasively by the Finapres.3. Heart rate (HR) increased during inspiration, with a nearly fixed time delay for mostVTand BF approximating 0.9 s. The magnitude of RS A increased with increases inVTand with decreases in BF. SBP decreased during inspiration, with a time delay which increased as BF decreased, resulting in a phase delay approximating 160°. The magnitude of the inspiratory fall in SBP increased with increases inVT. Increased amplitudes of RSA and SBP variation occurred at the lowest BF, consistent with the possibility of interactions between respiratory‐related influences and those due to ‘slow waves’ of vasomotor tone.4. The present results are consistent with the conclusion that respiratory effects on SBP are caused by a mechanism other that simply cha

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb01643.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1. 11β‐Hydroxysteroid dehydrogenase (11‐HSD) activity in mesenteric arteries of spontaneously hypertensive rats (SHR) and Wistar‐Kyoto (WKY) rats was determined and expressed as the percentage conversion of [3H]‐corticosterone to [3H]‐11‐dehydrocorticosterone.2. 11‐HSD activity was significantly decreased in mesenteric arteries of both 4 and 9 week old SHR (8.4 ± 0.8%, 5.0 ± 1.5%, respectively) compared with WKY rats (12.4 ± 0.6%, 15.8 ± 0.7%, respectively;P≤ 0.05).3. Total RNA from rat vascular smooth muscle cells (VSMC) and endothelial cells (EC) were prepared with selective precipitation in 3 mol/L LiC1/6 mol/L urea. The expression of 11‐HSD mRNA was confirmed in the rat VSMC but its mRNA expression was not detected in EC, using northern blot analysis.4. The results in this study indicate that 11‐HSD in the vascular wall may play a role in the pathogenesi

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb01644.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1. The effects of hydroxocobalamin (Vitamin B12a) on relaxations produced by nitric oxide (NO), some NO‐donating compounds and nitrergic nerve stimulation in isolated preparations of the rat anococcygeus muscle were compared with the effects of haemoglobin.2. Hydroxocobalamin (30 μmol/L) significantly reduced relaxations induced by NO (0.1–3 μmol/L) and sodium nitroprusside (SNP; 0.01–0.3 μmol/L) but did not affect relaxations induced by glyceryl trinitrate (GTN; 0.01–1 μmol/L), S‐nitrosocysteine (0.1–0.3 μmol/L) or stimulation of nitrergic nerves. A higher concentration of hydroxocobalamin (100 μmol/L) slightly reduced nitrergic nerve stimulation‐induced relaxations.3. Haemoglobin (10 μmol/L) blocked relaxation induced by NO and reduced relaxations induced by SNP, GTN, S‐nitrosocysteine and nitrergic nerve stimulation.4. When nitrergic nerve stimulation‐induced relaxations had been partially reduced by the NO synthase inhibitor l‐NAME (5–10 μmol/L), hydroxocobalamin had only a weak and transient inhibitory effect.5. Noradrenergic contractions induced by field stimulation were not affected by hydroxocobalamin (30 μmol/L), but were enhanced by haemoglobin (10 μmol/L).6. The results suggest that the transmitter released from nitrergic nerves in anococcygeus muscles resembles NO‐releasing compounds such as S‐nitrosocyst

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb01645.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1. The purpose of the present study was to investigate the effects of Ca2+‐antagonists (verapamil and diltiazem) on dopamine release in the central nervous system in hypertension.2. Striatal slices obtained from spontaneously hypertensive rats (SHR) and Wistar‐Kyoto (WKY) rats were prelabelled with [3H]‐dopamine, and superfused with Krebs‐Ringer solutionin vitro. The slices were stimulated electrically at a frequency of 1 Hz.3. Stimulation‐evoked release of [3H]‐dopamine from striatal slices was significantly decreased in SHR compared with WKY rats.4. Exposure of slices to verapamil and diltiazem significantly increased the stimulation‐evoked [3H]‐dopamine release. The facilitatory effects of the Ca2+‐antagonists on dopamine release were significantly greater in SHR than in WKY rats.5. Because central nervous system dopaminergic mechanisms appear to be depressor, the results suggest that the pronounced effects of verapamil and diltiazem on dopamine release in SHR might be involved in the central hypotensive mechanisms of the

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb01646.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1. The hypothesis that adrenocorticotrophin (ACTH)‐induced hypertension is a consequence of steroid‐induced hyperinsulinaemia was tested using the somatostatin analogue (sandostatin, octreotide) to inhibit insulin release in Sprague‐Dawley (SD) rats (n= 41).2. Octreotide (20 μg, twice daily) did not modify blood pressure, plasma glucose, bodyweight, water and electrolyte balance, or organ weights but inhibited insulin secretion in the SD rat.3. Compared with sham injection, ACTH‐treated (0.5 mg/kg per day) SD rats showed an increase in blood pressure (sham 111 ± 4 mmHg; ACTH 140 ± 5 mmHg on treatment day 10 (P≤ 0.01), organ weights, water intake, urine volume, plasma glucose, insulin and sodium concentrations, and decrease of bodyweight and plasma potassium concentration.4. Systolic blood pressure in rats treated with combined octreotide and ACTH was similar to that in rats on ACTH alone. Plasma insulin concentration was lower in octreotide + ACTH treated rats than with ACTH treatment alone. There were no differences in body or organ weights, plasma glucose, water or electrolyte balance.5. Octreotide lowered plasma insulin concentration to the normal range but did not modify ACTH‐induced hypertension in SD rats. These data do not support the notion that insulin‐mediated alterations in blood pressure are a major mechanism for ACTH‐induced hyper

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb01647.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1. Experiments were designed to determine the effects of low concentrations (5–500 nmol/L) of naftidrofuryl, a 5‐hydroxytryptamine (5‐HT) antagonist, on renal functions and prostanoid synthesis responses to noradrenaline (NA) and 5‐HT. Isolated kidneys of 8 week old male spontaneously hypertensive rats were perfused at a constant flow rate in a single‐pass system.2. In baseline conditions, naftidrofuryl did not modify the renal vascular resistance and the glomerular filtration rate (GFR), although it elicited a significant but not dose‐dependent increase in the venous excretion of 6‐keto‐prostaglandin (PG) F1αand thromboxane (Tx)B2, the stable end‐products of PGI2and TxA2, respectively.3. NA increased renal vascular resistance and GFR in a dose‐dependent manner and enhanced the venous excretion of 6‐keto‐PGF1αand TxB2. Naftidrofuryl significantly attenuated the effects of NA on renal vascular resistance, abolished those on GFR and enhanced, at the highest concentration (500 nmol/L) only, those on 6‐keto‐PGF1αexcretion.4. 5‐HT increased renal vascular resistance but not GFR. It did not change the sodium excretion and the release of 6‐keto‐PGF1αand TxB2. Naftidrofuryl blunted the RVR response to 5‐HT without change in the prostanoid release. The inhibitory action of naftidrofuryl was not modified by indomethacin which, by itself, prevented the vasoconstrictor response to 5‐HT.5. It is concluded that, in isolated perfused kidneys of SHR, naftidrofuryl inhibits the contractile response to 5‐HT and NA; this effect is not dependent upon changes in synthesis of PGI2or TxA2and the vasoconstrictor effect of 5‐HT involves the release of a cyc

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb01648.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SUMMARY1. This study aimed to examine whether a high salt diet alters control of vascular resistance by arterial baroreflex and vagal afferents in spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY).2. SHR and WKY aged 8 weeks were fed either high (8%) or normal salt (0.4%) diet for 4 weeks. Arterial baroreflex control of hindlimb vascular resistance was assessed by examining reflex‐induced vasodilation and vasoconstriction in response to phenylephrine and nitroprusside, respectively, in the constant‐flow perfused hindlimb of urethane‐anesthetized rats.3. Tonic influence of the cardiopulmonary vagal afferents was evaluated by examining the effects of vagotomy on hindlimb vascular resistance and on the gain of arterial baroreflex control of hindlimb vascular resistance.4. The gain of the arterial baroreflex control of hindlimb vascular resistance in response to both phenylephrine and nitroprusside were not significantly different between SHR receiving high and normal salt diets, and between WKY receiving high and normal salt diets.5. Vagotomy increased hindlimb vascular resistance in all four groups of rats. However the magnitude of the increase in hindlimb vascular resistance was less in SHR on a high salt diet than those in SHR on a normal salt diet but similar between the two groups of WKY. Vagotomy increased the slope of arterial baroreflex control of hindlimb vascular resistance in SHR receiving a normal salt diet and the two groups of WKY but not in SHR receiving a high salt diet.6. These results suggest that a high salt diet attenuates the inhibitory influence of vagal afferents on the control of vascular resistance in SHR but not in WKY, while the arterial baroreflex control of vascular resistance is preserved during high salt diet in both SHR an

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb01649.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1993.tb01650.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY