Search PubMed⌕ Search

Biomedical subjects

T Bennett

Publications and source records attributed to T Bennett.

At least 181 records · Page 10Linked to original sources
PubMed1992

Feasibility of an implantable arrhythmia monitor.

Conventional Holter monitoring is of limited benefit in patients with infrequent symptoms suspected to be related to arrhythmia. A small recorder implanted subcutaneously might obviate many limitations of conventional monitoring. To determine the feasibility of obtaining adequate electrocardiographic signals from such a device, a prototype was temporarily implanted in 17 patients undergoing pacemaker implantation. The prototype contained four disc-shaped titanium electrodes, 0.21 inches in diameter embedded in epoxy. The four electrodes were in a square configuration spaced 0.72 inches center to center and were placed face down in a subcutaneous pocket in the left pectoral region. Bipolar recordings were made from a horizontal pair, a vertical pair, and both diagonal paris of electrodes (interelectrode distance 1.02 inches) and recorded on electromagnetic tape after filtering at 0.5-250 Hz. The mean peak-to-peak amplitude in each configuration was determined over a five-beat interval. Clear recordings were obtained from all 17 patients with recognizable P, QRS, and T waves. The amplitude of the signals obtained from the diagonal pairs of electrodes (175 +/- 51 and 170 +/- 54 microV) were greater than obtained from either the vertical pair (142 +/- 62 microV, P = 0.08 compared to diagonal electrodes) or the horizontal pair of electrodes (105 +/- 54 microV, P < 0.01). The maximum amplitude recorded from any configuration was 189 +/- 54 microV. In six patients the device was also tested with the electrodes face up in the subcutaneous pocket.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Differences in hospital resource allocation among sick newborns according to insurance coverage.

OBJECTIVE: To assess whether newborns' insurance coverage was associated with differences in the allocation of hospital services. DESIGN: Retrospective analysis of computerized hospital discharge data, comparing resource allocation among newborns according to insurance status, controlling for race/ethnicity, diagnoses, hospital characteristics (ownership, teaching status, nursery level), and disposition. SETTING: All California civilian acute-care hospitals. PATIENTS: Population-based sample, excluding out-of-hospital and military hospital births. Resource allocation was studied among all newborns discharged in 1987 with evidence of serious problems (N = 29,751). MAIN OUTCOME MEASURES: Length of stay, total charges, and charges per day. RESULTS: Sick newborns without insurance received fewer inpatient services than comparable privately insured newborns with either indemnity or prepaid coverage. This pattern was observed across all hospital ownership types. Mean stay was 15.7 days for all privately insured newborns (15.6 days for those with indemnity and 15.7 days for those with prepaid coverage), 14.8 days for Medicaid-covered newborns, and 13.2 days for uninsured newborns (P less than .001). Length of stay, total charges, and charges per day were 16%, 28%, and 10% less, respectively, for the uninsured than for all privately insured newborns (P less than .001). Resources for newborns covered by Medicaid were generally greater than for the uninsured and less than for the privately insured. Both uninsured and Medicaid-covered newborns were found to have more severe medical problems than the privately insured. CONCLUSIONS: The findings cannot be explained by differences in medical need or by differences in non-medically indicated services; they constitute prima facie evidence of inequities that need to be addressed by policy changes.

California↗
PubMed1991

Human alpha-calcitonin gene-related peptide (CGRP)-(8-37), but not -(28-37), inhibits carotid vasodilator effects of human alpha-CGRP in vivo.

Human alpha-calcitonin gene-related peptide-(8-37) alone (up to doses of 30 nmol kg-1 min-1) had no significant effects on blood pressure, heart rate or common or internal carotid haemodynamics, although it caused significant, reversible, inhibition of the hypotensive, tachycardic, and common and internal carotid vasodilator effects of human alpha-CGRP (0.03 nmol kg-1 min-1) in conscious, Long Evans rats. Human alpha-CGRP-(28-37) up to doses of 300 nmol kg-1 min-1 had no cardiovascular effects itself and did not influence responses to human alpha-CGRP. These results are consistent with the carotid haemodynamic effects of human alpha-CGRP being due largely to activation of the CGRP1-receptor subtype.

Animals↗
PubMed1991

Haemodynamic responses to nonhypotensive central hypovolaemia induced by lower body negative pressure in men and women.

Haemodynamic responses to low levels of lower body negative pressure (LBNP) were investigated in two groups of healthy, normotensive volunteers (8 men and 8 women) during two repeated experimental runs on two occasions, the latter determined by the different phases of the menstrual cycle in the women. The data consisted of systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean blood pressure (MBP), pulse rate (fc), forearm blood flow (FBF) and forearm vascular conductance (FC). The resting cardiovascular status was similar in men and women, except that women had a significantly higher fc than men. LBNP (1.3, 2.7 and 4 kPa) had no significant effect on any BP variable or on fc. However, FBF and FC were reduced at all levels of LBNP. Significant overshoots in FBF and FC were seen in all subjects following the release of LBNP of 2.7 and 4 kPa and, in most cases, after release of LBNP of 1.3 kPa. There were no significant gender differences in any of the responses to LBNP. Furthermore, none of the cardiovascular variables measured showed significant differences between the follicular and luteal phases of the menstrual cycle in women, either at rest or during exposure to LBNP, and the responses in the men on the two occasions were not different. These findings indicate that gender differences in responses to LBNP hypothesized previously are not apparent during and after exposure to low levels of LBNP.

Adult↗
PubMed1991

Differential regional haemodynamic effects of the non-peptide angiotensin II antagonist, DuP 753, in water-replete and water-deprived Brattleboro rats.

Regional haemodynamic effects of DuP 753 were assessed in conscious unrestrained Brattleboro (i.e. vasopressin-deficient) rats, chronically instrumented with miniaturised pulsed Doppler flow probes and intravascular catheters. Responses to DuP 753 were assessed in water-replete animals and in animals following 14h water deprivation to render cardiovascular status dependent on the renin angiotensin system (RAS). In water-replete animals DuP 753 had little effect on mean arterial blood pressure, but there were dose-dependent tachycardias and increases in renal blood flow, associated with vasodilatations. There were also increases in mesenteric blood flow and vascular conductance, but these were not clearly dose-related; DuP 753 had no significant effects on hindquarters haemodynamics. In water-deprived animals DuP 753 caused dose-dependent hypotension, tachycardia, and renal and mesenteric vasodilatations; hindquarters vasodilatation was not dose-dependent. In both conditions, in the presence of DuP 753 (10 mg/kg), captopril had little additional effect. DuP 753 appears to be an extremely effective tool for assessing the role of the RAS in cardiovascular regulation.

Angiotensin II↗
PubMed1991

Cardiovascular reflex responses in Bangladeshi and European subjects.

1. Cardiovascular responses to three different interventions, namely the Valsalva manoeuvre, deep breathing and a cold stimulus on the face, were studied in two ethnic groups (European and Bangladeshi) that have been shown to differ in the prevalence of hypertensive-vascular disease. The data obtained consisted of systolic blood pressure, diastolic blood pressure, mean blood pressure, heart rate measured by using a beat-by-beat non-invasive blood pressure monitor (the Finapres), forearm blood flow determined by venous occlusion plethysmography, and calculated forearm vascular resistance. 2. The resting haemodynamic status was similar in European and Bangladeshi subjects. However, Bangladeshi subjects showed a greater increase in heart rate, but only after 20 s into the Valsalva manoeuvre, and greater overshoots in mean blood pressure after the manoeuvre than the European subjects. Furthermore, after cold face stimulation the fall in forearm vascular resistance to baseline levels was delayed in Bangladeshi subjects relative to that in the European subjects. 3. There were no inter-group differences in the reflex bradycardia relative to mean blood pressure or in the cardiac baroreflex sensitivity estimated from systolic blood pressure and pulse interval after the Valsalva manoeuvre. In addition, values for the mean difference between maximum and minimum pulse intervals during deep breathing did not differ in Bangladeshi and European subjects. 4. These findings together suggest that, although cardiac vagal reflex responses appear similar in the two groups, sympatho-adrenal influences on the heart and vasculature may be greater in Bangladeshi subjects than in European subjects.

Adult↗
PubMed1991

The effects of endothelin-1 and NG-nitro-L-arginine methyl ester on regional haemodynamics in conscious rats with streptozotocin-induced diabetes mellitus.

1. Resting haemodynamic status and responses to endothelin-1 (0.0004, 0.04, 0.4 nmol kg-1) and NG-nitro-L-arginine methyl ester (L-NAME, 10 mg kg-1) were assessed in conscious, Wistar rats treated with streptozotocin (STZ) to induce diabetes mellitus, and in control animals treated with saline. 2. In the resting state, STZ-treated rats had a bradycardia relative to control animals (291 +/- 13 and 337 +/- 10 beats min-1, respectively), but mean arterial blood pressures were the same in the two groups (STZ-treated 109 +/- 3; control 114 +/- 4 mmHg). However, the STZ-treated rats had raised renal (105 +/- 9 units) and mesenteric (114 +/- 16 units) vascular conductances and reduced hindquarters vascular conductance (26 +/- 4 units) relative to control rats (renal, 80 +/- 6; mesenteric, 75 +/- 7; hindquarters, 37 +/- 3 units). 3. Increasing doses of endothelin-1 caused similar, early falls and subsequent rises in mean arterial blood pressures in both groups of rats. Although there were initial hindquarters vasodilatations with endothelin-1 that were not different in STZ-treated and control rats, there were subsequent renal and mesenteric vasoconstrictions that were greater in the former. Hence, the similar rises in mean arterial blood pressures must have been accompanied by a greater reduction in cardiac output in the STZ-treated rats. 4. L-NAME caused similar renal and mesenteric vasoconstrictions in control and STZ-treated rats, but there was a smaller pressor effect and an attenuated hindquarters vasoconstrictor response to L-NAME in STZ-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Selective impairment of hindquarters vasodilator responses to bradykinin in conscious Wistar rats with streptozotocin-induced diabetes mellitus.

1. Male, Wistar rats were treated with streptozotocin (STZ, 70 mg kg-1, i.p.) or saline and chronically instrumented with pulsed Doppler probes and intravascular catheters (implanted under sodium methohexitone anaesthesia) to allow assessment of haemodynamics in the conscious state 28 days later. 2. Control and STZ-treated rats received bolus doses of glyceryl trinitrate (10-80 nmol kg-1), acetylcholine (0.1-5 nmol kg-1) and bradykinin (0.3-30 nmol kg-1). 3. Although, as reported previously, STZ-treated rats had normal mean arterial blood pressure together with renal and mesenteric vasodilatations and hindquarters vasoconstriction relative to control rats, both groups showed similar hypotensive and regional haemodynamic responses to glyceryl trinitrate and acetylcholine. However, while the depressor effects of bradykinin were similar in control and STZ-treated rats, the former showed a hindquarters vasodilator response to bradykinin that was absent in the STZ-treated rats. 4. A loss of bradykinin-mediated vasodilatation in the hindquarters vascular bed in STZ-treated rats in the presence of normal, hindquarters vasodilator responses to other agents and normal bradykinin-mediated vasodilator responses in other vascular beds is consistent with existing evidence that the vasodilatation elicited by bradykinin in the hindquarters vascular bed is particularly dependent on nitric oxide synthesis and that this is impaired selectively in STZ-treated rats.

Acetylcholine↗
PubMed1991

Differential effects of (+/-)-dobutamine and human alpha-CGRP on cardiac and on regional haemodynamics in conscious Long Evans rats.

1. Comparisons were made of the full haemodynamic profiles of the known cardiostimulant, (+/-)-dobutamine, and the putative inotropic peptide, human alpha-calcitonin gene-related peptide (human alpha-CGRP), in conscious, chronically-instrumented Long Evans rats. Both substances were administered continuously i.v. for 60 min at two doses ((+/-)-dobutamine, 2 and 10 mumol kg-1 h-1; human alpha-CGRP, 0.15 and 1.5 nmol kg-1 h-1). 2. In spite of their similar (small) effects on mean arterial blood pressure, the low doses of (+/-)-dobutamine and human alpha-CGRP influenced cardiac haemodynamics differently. Thus, (+/-)-dobutamine caused an increase in cardiac index (due to a tachycardia), accompanied by rises in peak aortic flow, maximum rate of rise of aortic flow (dF/dtmax) and total peripheral conductance. However, the latter waned during the infusion, and after the infusion there was a significant systemic vasoconstriction and reductions in peak aortic flow, dF/dtmax and stroke index. Such 'off' effects following dobutamine infusion have not been described previously. The infusion of the lower dose of human alpha-CGRP caused only a transient fall in central venous pressure. 3. The rise in total peripheral conductance during infusion of the lower dose of (+/-)-dobutamine was associated with increases in hindquarters and common and internal carotid vascular conductances. The fall in total peripheral conductance after infusion was associated with renal vasoconstriction. Although there was no significant change in total peripheral conductance during the infusion of the lower dose of human alpha-CGRP there were hindquarters and carotid vasodilatations together with mesenteric vasoconstriction. 4. Infusion of the higher dose of ( )-dobutamine had greater effects than the lower dose on all cardiac haemodynamic variables and additionally, increased stroke index. However, the negative cardiac haemodynamic effects following the offset of infusion were also enhanced in association with marked renal and mesenteric vasoconstrictions. While infusion of the higher dose of human alpha-CGRP increased cardiac index, peak aortic flow, dF/dtmax and total peripheral conductance, stroke index fell together with central venous pressure. 5. (+/-)-Dobutamine caused greater cardiostimulation and increases in hindquarters blood flow than did human alpha-CGRP. However, the latter at the higher dose caused substantially greater common and internal carotid hyperaemia than did (+/-)-dobutamine, possibly indicating a selective and additional effect of human alpha-CGRP on cranial blood flow. Furthermore, there were no adverse cardiovascular effects following infusion of human alpha-CGRP.

Animals↗
PubMed1991

Regional haemodynamic effects of prolonged infusions of human alpha-calcitonin gene-related peptide in conscious, Long Evans rats.

1. Haemodynamic measurements were made in conscious, Long Evans rats chronically instrumented for the assessment of changes in regional blood flows (renal, mesenteric and hindquarters, or internal and common carotid) and systemic arterial blood pressure and heart rate, before, during and after 3 day infusions of vehicle or human alpha-calcitonin gene-related peptide (CGRP) (1.5 or 15 nmol kg-1 h-1). 2. In animals with renal, mesenteric and hindquarters flow probes (n = 8), during the first day of infusion of human alpha-CGRP (1.5 nmol kg-1 h-1) there was sustained tachycardia and hypotension, a sustained reduction in renal flow, a transient reduction in mesenteric flow and a relatively well-maintained increase in hindquarters flow. All these effects were significantly different from the changes seen in vehicle-infused rats (n = 8), but calculation of vascular conductances showed only the late mesenteric vasodilatation and the sustained hindquarters vasodilatation were different from the changes in vehicle-infused rats. However, by the second day of infusion and thereafter cardiovascular variables in the animals receiving vehicle and those receiving human alpha-CGRP were not different. 3. Nine animals instrumented with probes to monitor changes in internal and common carotid haemodynamics initially received human alpha-CGRP infused at a rate of 1.5 nmol kg-1 h-1. Three of these animals still showed some response to the human alpha-CGRP (tachycardia, hypotension, hyperaemic vasodilatation) throughout the second day of infusion and hence were taken through the 3 day infusion protocol. When the infusion was stopped on the fourth day all these animals showed reversal of the effects of human alpha-CGRP. 4. The results indicate substantial inter-individual variation in the haemodynamic effects of prolonged infusions of human alpha-CGRP in conscious, Long Evans rats. However, since increasing the dose of human alpha-CGRP overcame the desensitization, it is feasible that, in the clinical setting, maintained increases in internal carotid blood flow could be achieved by individually-adjusted infusions of human alpha-CGRP.

Animals↗
PubMed1991

Cardiac haemodynamic effects of the non-peptide, angiotensin II-receptor antagonist, DuP 753, in conscious Long Evans and Brattleboro rats.

1. In previous experiments in conscious, water-replete Long Evans and Brattleboro rats the non-peptide angiotensin II-receptor antagonist, DuP 753, caused only slight hypotension and peripheral (particularly renal) vasodilatations. However in water-deprived (i.e. renin-dependent) Brattleboro rats, DuP 753 caused marked hypotension and regional vasodilatations. The major objective of the present study was to determine if the hypotensive effects of DuP 753 under any of the experimental conditions studied previously were contributed to by negative effects on cardiac haemodynamics. 2. Male, Long Evans and Brattleboro rats were chronically instrumented with electromagnetic flow probes on the ascending aorta and with intravascular catheters. Data were collected by use of a microcomputer-based system that provided digitised print-out of instantaneous heart rate, mean arterial blood pressure, cardiac output, stroke volume, peak aortic flow, maximum positive slope of the aortic flow signal (+ dF/dtmax), total peripheral conductance and central venous pressure. 3. Incremental i.v. bolus doses (0.1-10 mg kg-1, at 15 min intervals) of DuP 753 were administered to water-replete Long Evans (n = 8) and Brattleboro (n = 8) rats, and to water-deprived (14 h) Brattleboro rats (n = 9) (the latter animals show marked activation of the renin-angiotensin system). In all groups, 15 min after the highest dose of DuP 753 had been given, a supramaximal dose of captopril (2 mg kg-1) was injected to determine if it had any additional effects. 4. In water-replete, Long Evans and Brattleboro rats, DuP 753 (0.1-1 mg kg-1) caused slight, transient hypotension, with rises in total peripheral conductance; increases in cardiac output, peak aortic flow, + dF/dtmax and stroke volume were inconsistent and central venous pressure did not change. Higher doses of DuP 753 (3 and 10mgkg-') caused modest, sustained hypotension that was due entirely to an increase in total peripheral conductance, since cardiac output, peak aortic flow and + dF/dtmax showed transient elevations; captopril had no additional hypotensive or vasodilator effects. 5. Under resting conditions, water-deprived Brattleboro rats showed an increase in mean arterial blood pressure, but there were reductions in total peripheral conductance, cardiac output and + dF/dtmax. DuP 753 (0.1-10 mg kg- 1, i.v., boluses at 15 min intervals) caused incremental hypotension and tachycardia and dose-dependent rises in total peripheral conductance that were accompanied by transient increases in cardiac output, peak aortic flow and + dF/dtmax; captopril had no additional hypotensive or vasodilator effects. 6. Under no conditions were there any negative effects of DuP 753 on myocardial function; moreover, it is likely the transient increases in cardiac function following DuP 753 were indirect and due to the reduction in afterload. Thus, it appears the haemodynamic effects of DuP 753 can be explained by its vasodilator action.

Angiotensin II↗
PubMed1991

Effects of NG-nitro-L-arginine methyl ester on vasodilator responses to acetylcholine, 5'-N-ethylcarboxamidoadenosine or salbutamol in conscious rats.

1. Conscious, Long Evans rats (n = 16), chronically instrumented for the measurement of regional haemodynamics were given 3 min, randomized infusions of two doses of sodium nitroprusside (1.5 and 15 micrograms min-1), acetylcholine (0.4 and 4 micrograms min-1), 5'-N-ethylcarboxamidoadenosine (NECA; 45 and 450 ng min-1), and salbutamol (24 and 240 ng min-1) in the absence and in the presence of NG-nitro-L-arginine methyl ester (L-NAME; 1 mg kg-1 h-1), a potent inhibitor of nitric oxide biosynthesis. 2. Sodium nitroprusside caused hyperaemic vasodilatation in the mesenteric, and common carotid vascular beds. These effects were enhanced in the presence of L-NAME, as was the hypotension. 3. Acetylcholine caused hyperaemic vasodilation inp6he renal, internal carotid and common carotid vascular beds. These effects were attenuated in the presence of L-NAME, but the hypotension was unaffected. 4. NECA caused hyperaemic vasodiltation in the renal, mesenteric, hindquarters, internal carotid and common carotid vascular beds. However, only the hindquarters and internal carotid responses were diminished in the presence of L-NAME and the hypotension was unchanged. 5. Salbutamol caused hyperaemic vasodilatation in the hindquarters vascular bed only. This effect was reduced in the presence of L-NAME, but the hypotension was unchanged. 6. The results indicate marked regional variations in the sensitivity of vasodilator responses to L-NAME that can depend on the vasodilator agent chosen and the dose employed. It is clear from these findings also that measurement of mean arterial blood pressure alone cannot provide adequate information on which to judge the involvement of L-NAME-sensitive mechanisms in vasodilator responses in vivo.

Acetylcholine↗
PubMed1991

Effects of NG-nitro-L-arginine methyl ester or indomethacin on differential regional and cardiac haemodynamic actions of arginine vasopressin and lysine vasopressin in conscious rats.

1. Measurements of changes in renal, mesenteric and hindquarters haemodynamics or cardiac haemodynamics in response to i.v. bolus doses of arginine vasopressin (AVP) or lysine vasopressin (LVP, 0.7 and 7.0 pmol) were made in conscious, chronically-instrumented Long Evans rats. 2. In some experiments AVP and LVP were administered during an infusion of NG-nitro-L-arginine methyl ester (L-NAME; 1.0 or 0.3 mg kg-1 h-1) to determine whether or not inhibition of nitric oxide production influenced the cardiovascular effects of the peptides. In other experiments, indomethacin (bolus dose of 5 mg kg-1 followed by infusion at 5 mg kg-1 h-1) was given to determine the possible involvement of cyclo-oxygenase products in the responses to AVP and LVP. 3. Under control conditions, the lower dose of LVP had significantly greater effects than AVP on heart rate, mean arterial blood pressure, renal, mesenteric and hindquarters conductances, total peripheral conductance, cardiac index, peak aortic flow and +dF/dtmax. The higher dose of LVP had significantly greater effects than AVP on all variables (i.e. including stroke index and central venous pressure). 4. In the presence of L-NAME (1 mg kg-1 h-1) there was a sustained increase in mean arterial blood pressure (+23 +/- 3 mmHg) and reductions in mesenteric (-38 +/- 4%) and hindquarters (-30 +/- 6%) vascular conductances. Under these conditions the difference in the pressor effects of AVP and LVP was abolished, but their differential effects on regional and cardiac haemodynamics persisted. This dose of L-NAME did not change cardiac baroreflex sensitivity. 5. During infusion of L-NAME at a lower rate (0.3mgkg-th-1), baseline cardiovascular status was unchanged and regional haemodynamic effects of AVP and LVP were enhanced, but the differences in the regional vasoconstrictor responses to the two peptides persisted. 6. Indomethacin (5 mg kg-1 bolus, then 5 mg kg- 'h-1 infusion) augmented the renal vasoconstrictor responses to AVP and LVP, but abolished the difference in the hindquarters vasoconstrictor responses to the two peptides. However, the differences in the pressor and the renal and mesenteric vasoconstrictor effects of AVP and LVP still occurred in the presence of indomethacin. 7. The results indicate that AVP normally has lesser cardiovascular effects than LVP but this difference does not seem to be due to more effective stimulation of nitric oxide-mediated or cyclo-oxygenase-dependent vasodilator mechanisms by AVP than LVP.

Animals↗
PubMed1991

Mechanisms contributing to the differential haemodynamic effects of bombesin and cholecystokinin in conscious, Long Evans rats.

1. Long Evans rats were chronically instrumented with intravascular catheters and pulsed Doppler probes to assess changes in renal, mesenteric and hindquarters blood flows and vascular conductances in response to bombesin (2.5 micrograms kg-1, i.v.) and cholecystokinin (CCK) (0.5 and 5.0 micrograms kg-1, i.v.). 2. Bombesin caused an increase in heart rate and blood pressure, together with a transient renal vasoconstriction and prolonged mesenteric vasodilatation; there was an early hindquarters vasodilatation followed by vasoconstriction. 3. In the presence of phentolamine, bombesin caused a fall in blood pressure due to enhanced hindquarters vasodilatation; these effects were reversed by propranolol and hence were possibly due to circulating adrenaline acting on vasodilator beta 2-adrenoceptors. 4. During concurrent administration of phentolamine, propranolol and atropine, bombesin caused prolonged tachycardia and a rise in blood pressure. The renal vasoconstrictor and mesenteric vasodilator effects of bombesin were not reduced under these conditions and thus probably were direct and/or indirect non-adrenergic, non-cholinergic (NANC) effects. 5. CCK caused dose-dependent increases in blood pressure accompanied by renal, mesenteric and hindquarters vasoconstriction followed, after the higher dose, by vasodilatations. The lower dose of CCK increased heart rate but there was a bradycardia followed by a tachycardia after the higher dose. 6. Experiments with antagonists as described above indicated the pressor effect of CCK was mediated largely through alpha-adrenoceptors, as were the mesenteric and hindquarters vasoconstrictor effects; CCK exerted NANC negative chronotropic effects. 7. All the effects of CCK were markedly inhibited by L364,718. This observation, and the finding that L364,718 had no effect on the responses to bombesin, together with the dissimilarities in the regional haemodynamic effects of exogenous CCK and bombesin, indicate that the cardiovascular actions of the latter were not dependent on the release of endogenous CCK.

Animals↗
PubMed1991

Haemodynamic effects of human alpha-calcitonin gene-related peptide following administration of endothelin-1 or NG-nitro-L-arginine methyl ester in conscious rats.

1 We investigated the peripheral haemodynamic effects of human alpha-calcitonin gene-related peptide (CGRP) following administration of endothelin-1 or NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide production, in conscious, chronically-instrumented, Long Evans rats. 2 Infusion of endothelin-1 (3 nmol kg-1 h-1) caused hypertension, bradycardia and renal, mesenteric and hindquarters vasoconstrictions. Co-infusion of human alpha-CGRP (1.5 nmol kg-1 h-1) reduced the hypertension and abolished the hindquarters vasoconstriction caused by endothelin-1 but the renal and mesenteric vasoconstrictor actions of endothelin-1 were not affected. 3 Infusion of human alpha-CGRP (15 nmol kg-1 h-1) in the presence of endothelin-1 caused hypotension and hyperaemic vasodilatation in the hindquarters; the mesenteric vasoconstrictor effects of endothelin-1 were diminished, but there was only a transient reversal of the renal vasoconstrictor effects of endothelin-1. 4 Pretreatment with the non-peptide angiotensin II receptor antagonist, DuP 753 (10 mg kg-1), caused slight hypotension associated with renal, mesenteric and hindquarters vasodilatations, but DuP 753 did not affect responses to endothelin-1 infusion. However, under these conditions co-infusion of human alpha-CGRP (15 nmol kg-1 h-1) caused a sustained reversal of the renal vasoconstrictor effects of endothelin-1. 5 These results indicate that the failure of human alpha-CGRP to cause sustained reversal of the renal vasoconstrictor effects of endothelin-1 in the absence of DuP 753 was due to activation of the reninangiotensin system (possibly as a consequence of the hypotension). 6. In the second experiment, L-NAME (l0mgkg-1) caused renal, mesenteric and hindquarters vasoconstrictions similar to those seen in the presence of endothelin-1. However, the renal vasoconstrictor effects of L-NAME were reversed completely by human alpha-CGRP (l5nmolkg- h-1), even though the latter caused hypotension comparable to that seen in the presence of endothelin-1. These results are consistent with a lack of functional activation of the renin-angiotensin system by human alpha-CGRP in the presence of L-NAME. 7. The vasoconstrictor effects of L-NAME on the hindquarters were completely reversed by infusion of human alpha-CGRP, but hindquarters flow and vascular conductance did not rise above baseline levels. Hence these results indicate the hindquarters hyperaemic vasodilator effects of human alpha-CGRP seen in the presence of endothelin-1 were contributed to by nitric oxide-mediated mechanisms.

Angiotensin II↗