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T Bennett

Publications and source records attributed to T Bennett.

At least 73 records · Page 4Linked to original sources
PubMed1995

Haemodynamic effects of losartan and the endothelin antagonist, SB 209670, in conscious, transgenic ((mRen-2)27), hypertensive rats.

1. Hypertensive transgenic (TGR(mRen-2)27) (abbreviated to TG) rats (n = 6) and their normotensive Sprague-Dawley (SD) control strain (n = 7) were chronically instrumented for the measurement of cardiac haemodynamics. The hypertension in TG rats (mean blood pressure 181 +/- 9 mmHg) was entirely attributable to a reduction in total peripheral conductance (TG rats = 169 +/- 7, SD rats = 292 +/- 15 microliters min-1 mmHg-1 100g-1) since cardiac index was not different in the two strains (TG rats = 30.5 +/- 1.2, SD rats = 29.5 +/- 1.6 ml min-1 100g-1). 2. In other animals instrumented for the assessment of regional haemodynamics, the extent of peripheral vasoconstriction was similar in renal, mesenteric and hindquarters vascular beds in the TG rats (reduction in vascular conductance relative to SD rats = 42%, 46% and 49%, respectively). 3. During an 8 h observation period with saline infusion, or following injection of losartan (10 mg kg-1) in SD rats there was no hypotension or regional vasodilation. With infusion of the endothelin antagonist, SB 209670 (10 micrograms kg-1 min-1), there was a slight hypotension, but no significant vasodilation; co-administration of losartan and SB 209670 caused a similar profile of effect, although the hypotension was increased. 4. With the same experimental protocol in TG rats, losartan caused a biphasic, progressive fall in mean arterial blood pressure accompanied by renal, mesenteric and hindquarters vasodilation. Although the response to SB 209670 was not biphasic, its hypotensive and vasodilator effects were not different from those of losartan after 8 h. In the combined presence of losartan and SB 209670, mean arterial blood pressure (116 +/- 5 mmHg) was significantly lower than with SB 209670 (132+/-4 mmHg) or losartan(136 +/- 6 mmHg) alone, and renal, mesenteric and hindquarters vascular conductances (61 +/- 3, 90+/-14 and 52+/-4 [kHz nmHg-1]103, respectively) were higher than the corresponding values following either SB 209670 (49 +/- 4, 52 +/- 4 and 34 +/- 3 [kHz mmHg- 1]103, respectively) or losartan (43 +/- 5, 59 +/- 13 and 35+/-4 [kHz mmHg-1]103, respectively) alone. These results indicate the maintenance of hypertension inTG rats is dependent upon renal, mesenteric and hindquarters vasoconstriction, mediated by angiotensinII (AII) and endothelin (ET). Since we found that plasma ET-1 levels in TG rats (12.06+/-2.87 pmol 1-1)were lower than in SD rats (21.53 +/- 3.94 pmol 1-1), then it is possible that locally-generated, rather than circulating ET-l contributes to the widespread vasoconstriction in TG rats.

Angiotensin II↗
PubMed1995

Lack of effect of TNF antibodies on the cardiovascular sequelae of lipopolysaccharide infusion in conscious rats.

1. The aims of the present study were to determine the profile of tumour necrosis factor (TNF) release, and the effect of monoclonal antibodies to TNF, on the changes in regional haemodynamics and the responses to vasodilator and vasoconstrictor challenges, during a continuous 24 h low dose infusion of lipopolysaccharide (LPS) in conscious rats. 2. Male Long Evans rats were chronically instrumented for measurement of regional haemodynamics (renal, superior mesenteric and hindquarters) and were challenged with 3 min infusions of acetylcholine (22 nmol min-1), methoxamine (120 nmol min-1), salbutamol (0.83 nmol min-1) and bradykinin (14.4 nmol min-1). The rats were given either saline, or the TNF antibodies, TN3g1 or TN3g2a, 1 h before the start of a continuous infusion of LPS (150 micrograms kg-1 h-1) and were subsequently re-tested with the vasodilator and vasoconstrictor challenges 2, 6 and 24 h after the start of the LPS infusion. 3. Prior to infusion of LPS, TNF was not detectable in the plasma. During continuous infusion of LPS there was a transient elevation in plasma TNF levels, reaching a maximum (approximately 2300 pg ml-1) after approximately 1 h, and returning to undetectable levels after approximately 3 h of LPS infusion. 4. In the saline pretreated group, after 1-2 h of LPS infusion, there was a small hypotension and a marked renal vasodilation; 6 h after the start of LPS infusion there was a minor elevation in MAP above control levels, renal vasodilatation was maintained and a hindquarters vasoconstriction occurred; after 24 h of LPS infusion, there was a hypotension and renal and hindquarters vasodilatation. There were significant reductions in the tachycardic and renal vasodilator responses and an enhanced depressor response to acetylcholine after 24 h of LPS infusion. LPS infusion also caused a generalized hyporesponsiveness to the cardiovascular effects of methoxamine and salbutamol. The major changes in response to bradykinin were reduced tachycardic and enhanced depressor responses throughout the LPS infusion, a biphasic decrease and increase in renal conductance and enhanced hindquarters vasodilatation at 24 h. 5. Pretreatment with either TN3g1 or TN3g2a antibodies had no major effects on the changes in resting haemodynamics, or on the changes in response to methoxamine, salbutamol or bradykinin challenges during LPS infusion. However, the tachycardic responses to acetylcholine were generally preserved, and its hypotensive effect after 24 h of LPS infusion was not enhanced after TN3g1 or TN3g2a pretreatment. Thus, despite substantial, but transient, elevation of plasma TNF levels during continuous LPS infusion, it appears that the majority of cardiovascular changes were dependent on factors other than plasma TNF.

Acetylcholine↗
PubMed1995

Attenuation by creatine of myocardial metabolic stress in Brattleboro rats caused by chronic inhibition of nitric oxide synthase.

1. The present experiment was undertaken to investigate: (a) the effect of nitric oxide synthase (NOS) inhibition, mediated by oral supplementation of the NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), on measures of myocardial energy metabolism and function: (b) the effect of oral creatine supplementation on these variables, in the absence and presence of L-NAME. 2. In one series of experiments, 4 weeks oral administration of L-NAME (0.05 mg ml-1 day-1 in the drinking water) to Brattleboro rats caused significant reductions in myocardial ATP, creatine, and total creatine concentrations and an accumulation of tissue lactate when compared with control animals. Administration of creatine (0.63 mg ml-1 day-1 in the drinking water) for 4 weeks elevated myocardial creatine and total creatine concentrations and reduced lactate accumulation, but did not significantly affect ATP or phosphocreatine (PCr). Concurrent treatment with creatine and L-NAME prevented the reduction in creatine and total creatine concentrations, and significantly attenuated the accumulation of lactate and the reduction in ATP seen with L-NAME alone. 3. In a second series of experiments, 4 weeks treatment with L-NAME and creatine plus L-NAME increased mean arterial blood pressure in conscious Brattleboro rats. Hearts isolated from these animals showed decreased coronary flow and left ventricular developed pressure (LVDP), and total mechanical performance. Treatment with creatine alone had no measurable effect on either mean arterial blood pressure or coronary flow in isolated hearts. However, there was an increase in LVDP, but not in total mechanical performance, because there was a bradycardia. 4. These results indicate that creatine supplementation can attenuate the metabolic stress associated with L-NAME administration and that this effect occurs as a consequence of the action of creatine on myocardial energy metabolism.

Adenosine Triphosphate↗
PubMed1995

Enhancement of the haemodynamic effects of NG-monomethyl-L-arginine by transforming growth factor-beta 1 in conscious, normal, but not endotoxaemic, rats.

1. Male, Long Evans rats (350-450 g) were chronically instrumented for the measurement of regional haemodynamics, and the effects of TGF-beta 1 (25 micrograms kg-1 i.v. bolus) were assessed during infusion of saline (n = 9) or lipopolysaccharide (LPS, 150 micrograms kg-1 h-1; n = 12). In the same animals, responses to NG-monomethyl-L-arginine (L-NMMA 10 mg kg-1 bolus; 10 mg kg-1 h-1 infusion) were determined 18 h after administration of TGF-beta 1. In a separate experiment, the effects of the endothelin antagonist, SB 209670 (10 micrograms kg-1 min-1) on responses to TGF-beta 1 and to L-NMMA subsequently, were determined. 2. In the absence of LPS, TGF-beta 1 had slow-onset bradycardic and pressor effects accompanied by mesenteric and hindquarters, but not renal, vasoconstriction. Eighteen hours after TGF-beta 1, these effects had gone, but the bradycardic, pressor, and mesenteric vasoconstrictor responses to L-NMMA were enhanced. The haemodynamic changes following TGF-beta 1, and the augmentation of the subsequent responses to L-NMMA, were inhibited by SB 209670. These results are consistent with TGF-beta 1 stimulating the synthesis and release of endothelin, and an involvement of the latter in responses to L-NMMA. 3. The pressor effects of TGF-beta 1 were similar in LPS-infused and saline-infused animals, but in the former group the mesenteric vasoconstriction was enhanced and the hindquarters vasoconstriction diminished. Since, in the absence of TGF-beta 1, LPS-infused animals showed a developing hindquarters vasodilatation and mesenteric vasoconstriction, it is feasible that, in the presence of TGF-beta 1 and LPS together, the haemodynamic profile represented an amalgam of the individual effects of the two interventions, rather than a specific effect of TGF-beta 1 on the haemodynamic sequelae of endotoxaemia. 4. In the presence of LPS, haemodynamic responses to L-NMMA were suppressed, and TGF-beta 1 generally did not affect this suppression. A possible explanation of this observation is that LPS increased circulating endothelin levels, and thus resulted in desensitization to the effects of endothelin released following administration of L-NMMA.

Animals↗
PubMed1995

Cardiac and regional haemodynamics, inducible nitric oxide synthase (NOS) activity, and the effects of NOS inhibitors in conscious, endotoxaemic rats.

1. A reproducible model of the hyperdynamic circulatory sequelae of endotoxaemia in conscious, chronically-instrumented Long Evans rats, was achieved with a continuous infusion of lipopolysaccharide (LPS, 150 micro g kg(-1) h(-1)) for 32 h. Over the first 2 h of LPS infusion, there was a transient hypotension and tachycardia, accompanied by a marked increase in renal flow and vascular conductance, although there were reductions in cardiac and stroke index. Between 4-8 after the start of LPS infusion, there was slight hypotension and tachycardia, and a transient rise in mesenteric flow and conductance, but reductions in the hindquarters vascular bed; the hyperaemic vasodilatation in the renal vascular bed was maintained. At this stage, all cardiac haemodynamic variables were not different from baseline. At this stage, cardiac and stroke index were substantially elevated, in association with marked increases in peak aortic flow, dF/dtmax and total peripheral conductance; these changes were well-maintained over the following 8 h of LPS infusion. 2. By 2 h after the start of LPS infusion, only lung inducible nitric oxide synthase (iNOS) activity was increased, but at 6 h there were significant increases in iNOS activity in lung, liver, spleen, heart and aorta. (43.3 +/- 7.8, 28.8 +/- 3.3, 50.8 +/- 7.2, 3.04 +/- 0.29, 3.76 +/- 0.94 pmol min(-1) mg(-1) protein, respectively). However, by 24 h after the start of LPS infusion, iNOS activity was not elevated significantly in any tissue examined, and kidney iNOS activity did not change significantly during LPS infusion. Plasma nitrite/nitrate levels were increased after 2 h infusion of LPS (from 6.07 +/- 1.23 to 29.44 +/- 7.08 micromol l(-1)), and further by 6 h (228.10 +/- 29.20 micromol l(-1)), but were less 24 h after onset of LPS infusion (74.96 +/- 11.34 micromol l(-1)). Hence, the progressive hypotension, increasing cardiac function and developing hyperaemic vasodilatation in renal and hindquarters vascular beds between 8-24 h after the onset of LPS infusion, occurred when tissue iNOS activity and plasma nitrite/nitrate levels were falling. 3. Pretreatment with NG-monomethyl-L-arginine (L-NMMA, 30 mg kg(-1) bolus, 30 mg kg(-1) h(-1) infusion) 1 h before LPS infusion did not prevent the early hypotension, but abolished the initial renal vasodilatation and the later (6-8 h) fall in mean arterial pressure (MAP), and the additional renal vasodilatation.

Animals↗
PubMed1995

Enhancement of the hypotensive and vasodilator effects of endotoxaemia in conscious rats by the endothelin antagonist, SB 209670.

In conscious, chronically-instrumented rats, the non-selective endothelin antagonist, SB 209670 (10 micrograms kg-1 min-1), caused marked enhancement of the fall in mean arterial blood pressure during infusion of lipopolysaccharide (LPS) for 24 h (LPS alone = -6 +/- 3 mmHg; LPS+SB 209670 = -30 +/- 2 mmHg). This effect was accompanied by a conversion of the mesenteric vasoconstriction to a substantial mesenteric vasodilatation and an augmentation of the hindquarters vasodilatation, seen with LPS alone. Notably, the marked renal hyperaemic vasodilatation during LPS infusion was not affected significantly by SB 209670. These results indicate that endothelin, directly and/or indirectly, plays a pivotal role in the cardiovascular sequelae of endotoxaemia in conscious rats, and prevents marked hypotension, particularly by opposing mesenteric vasodilatation.

Animals↗
PubMed1995

Regional haemodynamic effects of human and rat adrenomedullin in conscious rats.

1. Male, Long Evans rats were chronically instrumented with pulsed Doppler flow probes and intravascular catheters to permit assessment of the regional haemodynamic responses to human and rat adrenomedullin, to compare the responses to human adrenomedullin to those of human alpha-CGRP in the absence and presence of the CGRP1-receptor antagonist, human alpha-CGRP [8-37], and to determine the involvement of nitric oxide (NO)-mediated mechanisms in the responses to human adrenomedullin, relative to human alpha-CGRP. 2. Human and rat adrenomedullin (0.3, 1, and 3 nmol kg-1, i.v.) caused dose-dependent hypotension and tachycardia, accompanied by increases in renal, mesenteric and hindquarters flows and vascular conductances. At the lowest dose only, the hypotensive and mesenteric vasodilator effects of rat adrenomedullin were significantly greater than those of human adrenomedullin. 3. Human alpha-CGRP at a dose of 1 nmol kg-1 caused hypotension, tachycardia and increases in hindquarters flow and vascular conductance, but reduction in renal and mesenteric flows, and only transient vasodilatations in these vascular beds. These effects were substantially inhibited by human alpha-CGRP [8-37] (100 nmol kg-1 min-1), but those of human adrenomedullin (1 nmol kg-1) were not; indeed, the mesenteric haemodynamic effects of the latter peptide were enhanced by the CGRP1-receptor antagonist. 4. In the presence of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 183 nmol kg-1 min-1), there was only a slight, but significant, inhibition of the hindquarters hyperaemic vasodilator effect of human adrenomedullin, but not that of human alpha-CGRP. 5. These results indicate that the marked regional vasodilator effects of human (and rat) adrenomedullin are largely independent of NO and, in vivo, do not involve CGRP1-receptors.

Adrenomedullin↗
PubMed1995

Physician directed networks: the Renaissance perspective.

It is time for all providers, physicians, hospital executives and ancillary providers to find creative ways to meet the healthcare needs of their local communities. More efficient systems of health care delivery will come from noncompetitive partnerships based on shared visions, collaborations, openess, honesty and integrity. RHP can be a catalyst for physicians and other providers in the Kansas City area and throughout the state to respond to the challenges and opportunities that lie before them.

Community Health Services↗
PubMed1994

Insurance-related differences in the risk of ruptured appendix.

BACKGROUND: We studied differences in the incidence of appendiceal perforation in patients with acute appendicitis according to their insurance coverage. METHODS: In a retrospective analysis of hospital-discharge data, we examined the likelihood of ruptured appendix among adults 18 to 64 years old who were hospitalized for acute appendicitis in California from 1984 to 1989. RESULTS: After controlling for age, sex, psychiatric diagnoses, substance abuse, diabetes, poverty, race or ethnic group, and hospital characteristics, we found that ruptured appendix was more likely among both Medicaid-covered and uninsured patients with appendicitis than among patients with private capitated coverage (odds ratios, 1.49 [95 percent confidence interval, 1.41 to 1.59] and 1.46 [95 percent confidence interval, 1.39 to 1.54], respectively). After adjustment for the above factors, the risk of appendiceal rupture associated with a lack of private insurance was elevated at both county and other hospitals, but admission to a county hospital was an independent risk factor. In all income groups, appendiceal rupture was more likely with fee-for-service than capitated private coverage (overall odds ratio, 1.20 [95 percent confidence interval, 1.15 to 1.25]). CONCLUSIONS: Among patients with appendicitis an increased risk of ruptured appendix may be due to insurance-related delays in obtaining medical care. Both organizational and financial features of Medicaid and various types or levels of private third-party coverage may be involved. The significant association between ruptured appendix and insurance coverage after adjustment for socio-economic differences suggests barriers to receiving medically necessary acute care that should be considered in current deliberations on health policy.

Adolescent↗
PubMed1994

Effects of angiotensin II AT1- or AT2-receptor antagonists on drinking evoked by angiotensin II or water deprivation in rats.

In previous studies, we found that central administration of the AT1-receptor antagonist, EXP 3174, and the AT2-receptor antagonist, PD 123319, blocked the cardiovascular response to centrally-injected angiotensin II (AII), although another AT2-receptor antagonist (PD 123177) was ineffective. In the present study, we examined the effects of these three compounds on the pressor and dipsogenic response to centrally-injected AII in conscious, male Long Evans rats, and the effect of EXP 3174 and PD 123319 on drinking in response to water-deprivation in Brattleboro rats. In Long Evans rats, AII-induced water intake and pressor effects were inhibited by EXP 3174 and PD 123319 (although with different time courses). In contrast, PD 123177 had little effect on the pressor response to i.c.v. AII, but enhanced its dipsogenic action. Following 8 h water deprivation in Brattleboro rats, neither EXP 3174 nor PD 123319 inhibited drinking when water was returned. These data indicate that EXP 3174 and PD 123319 inhibit thirst evoked by centrally injected AII, but not that caused by extracellular dehydration. In addition, since the putative AT2-receptor antagonists PD 123319 and PD 123177 have the opposite effects on i.c.v. AII-induced water intake, these results cannot be easily reconciled with a simple model of thirst in which AT2-receptors are involved in a final common pathway for drinking.

Angiotensin II↗
PubMed1994

Medical examiner data in injury surveillance: a comparison with death certificates.

Increasingly, researchers use medical examiner reports to study the epidemiology of fatal injuries, often assuming that reports of all fatal injuries are included in medical examiner databases. This study evaluated that assumption by comparing the medical examiner database with the death certificates of persons who died of fatal injuries in Iowa during 1990-1991. The authors also examined the association between demographic variables and the presence of a medical examiner report. Overall, medical examiners reported 68.7% of fatal injuries. Among broad categories of injury deaths, the percentages of medical examiner reports varied: 36.9% of fatalities from unintentional falls, 79.2% of transportation fatalities, 82.6% of intentional fatalities, and 57.3% of other external causes of death. Age and sex were also associated with the presence of a medical examiner report. Women's deaths were half as likely as men's to be reported by the medical examiner. Deaths among the elderly were underreported as well. Among the elderly, fatalities from unintentional falls and, to a lesser extent, transportation fatalities were less likely to be investigated by a medical examiner, but intentional fatalities were more likely to be. Although medical examiner reports may contain detailed information, they underreport the actual number of injury deaths. This underreporting is of special concern for injury research, since certain demographic groups were found to be underrepresented in medical examiner reports.

Accidental Falls↗
PubMed1994

Regional haemodynamic effects of carbachol injected into the hypothalamic paraventricular nuclei of conscious, unrestrained rats.

Carbachol was injected into the hypothalamic paraventricular nuclei (PVN) of conscious, unrestrained Long Evans rats, chronically instrumented with intravascular catheters and pulsed Doppler probes to assess changes in regional haemodynamics. Bilateral microinjections of carbachol (1 ng-1 microgram) produced increases in blood pressure, bradycardias and vasoconstrictions in renal, superior mesenteric and hindquarters vascular beds. In the presence of phentolamine, the bradycardic and hindquarters vasoconstrictor responses to carbachol were unchanged while the pressor response was smaller due to a reduction in the renal and the superior mesenteric vasoconstriction. In the presence of propranolol, the bradycardic response was reduced, but the pressor and renal vasoconstrictor responses were potentiated, whereas the superior mesenteric and hindquarter vasoconstrictions were not changed significantly. In the presence of phentolamine and propranolol, the heart rate and pressor responses, as well as the renal vasoconstriction, were unchanged, whereas the superior mesenteric vasoconstriction was reduced and the hindquarters vasoconstriction was potentiated. Together these results are consistent with an involvement of the sympathoadrenal system in the pressor response to carbachol injected into the PVN of untreated animals. They indicate that alpha-adrenoceptor-mediated vasoconstriction in the superior mesenteric vascular bed is a particularly important component in that regard. In the presence of the vasopressin antagonist, d(CH2)5(Tyr(Et))DAVP, alone or in combination with phentolamine and propranolol, the pressor response to carbachol was substantially reduced, while the renal and superior mesenteric vasoconstrictor effects were completely abolished; the bradycardia was not significantly affected by this treatment. These results indicate an important involvement of vasopressin in the cardiovascular responses to carbachol injected into the PVN of untreated animals. Moreover, in the presence of the vasopressin antagonist the hindquarters vascular bed showed a vasodilatation following PVN injection of carbachol; this effect was reversed to a vasoconstriction following combined i.v. pretreatment with the vasopressin antagonist, phentolamine and propranolol and hence was possibly due to circulating adrenaline acting on vasodilator beta 2-adrenoceptors. However, there was a residual hindquarters vasoconstriction raising the possibility that non-adrenergic, non-vasopressinergic vasoconstrictor mechanisms were influencing that vascular bed.

Adrenergic alpha-Antagonists↗
PubMed1994

Effects of an ET1-receptor antagonist, FR139317, on regional haemodynamic responses to endothelin-1 and [Ala11,15]Ac-endothelin-1 (6-21) in conscious rats.

1. In conscious, Long Evans rats, chronically instrumented for the measurement of regional haemodynamics, we compared responses to the putative, selective ETB-receptor agonist, [Ala1,3,11,15]endothelin-1 (ET-1), obtained from two sources (Microchemical Laboratory, Cambridge (MLC) and Neosystem Laboratory, France (NLF)). [Ala1,3,11,15]ET-1 (0.15, 0.3, 1 and 10 nmol kg-1) from MCL caused dose-dependent pressor effects, accompanied by reductions in renal and, particularly, mesenteric flows and vascular conductances; there was an initial hyperaemic vasodilatation in the hindquarters which was not dose-dependent, and only with the highest dose was there a subsequent vasoconstriction. There was no significant initial depressor response to [Ala1,3,11,15]ET-1 from MLC at any dose. However, the peptide from NLF exerted dose-dependent depressor and hindquarters vasodilator actions, and subsequent pressor effects. The difference between the two peptide preparations remains unexplained, but it appears that the [Ala1,3,11,15]ET-1 from MLC may activate ETB-receptors mediating vasoconstriction, more effectively than those mediating vasodilatation. 2. We also assessed responses to the putative ETB-receptor agonist, [Ala11,15]Ac-ET-1 (6-21) (BQ-3020), and determined the effects of the selective ETA-receptor antagonist, FR139317, on responses to ET-1 and BQ-3020 at doses matched for their initial depressor and subsequent pressor effects (ET-1, 0.5 nmol kg-1, BQ-3020, 10 nmol kg-1), and also at doses that did not affect mean arterial blood pressure, but which were matched for their renal vasoconstrictor effects (ET-1, 7.5 pmol kg-1; BQ-3020, 0.15 nmol kg-1). 3. BQ-3020 (0.15, 0.3 and 1 nmol kg-1) had dose-dependent pressor effects accompanied by reductions in renal and, particularly, mesenteric flows and vascular conductances. BQ-3020 at a dose of 10 nmol kg-1 elicited an initial depressor response which coincided with an attenuated mesenteric vasoconstrictor effect, accompanying a marked hindquarters vasodilatation. Hence, it appears that BQ-3020 may activate both vasoconstrictor and vasodilator ETB-receptors. 4. FR139317 (0.5 mumol kg-1) caused attenuation of the pressor, and renal, mesenteric and hindquarters vasoconstrictor effects of ET-1 (0.5 nmol kg-1) and of BQ-3020 (10 nmol kg-1), but the reductions of the pressor and renal vasoconstrictor effects of ET-1 were greater than those of BQ-3020. However, in the presence of FR139317, significant pressor and renal, mesenteric and hindquarters vasoconstrictor responses to ET-1 and BQ-3020 still occurred, and the initial depressor and hindquarters vasodilator responses to both peptides were unchanged. 5. ET-1 at a dose of 7.5 pmol kg-1 and BQ-3020 at a dose of 0.15 nmol kg-1 had similar renal vasoconstrictor effects. However, the response to ET-1 was almost abolished by FR139317 whereas that to BQ-3020 was unaffected. Moreover, under these conditions, the mesenteric vasoconstrictor and hindquarters vasodilator responses to ET-1 and to BQ-3020 were not changed by FR139317.6. Collectively, these results are consistent with the haemodynamic effects of ET-1 and BQ-3020 involving ETA-receptors or ETB-receptors, or ETA- and ETB-receptors, depending on the dose of agonist and the regional haemodynamic effect considered.

Animals↗