Intrarenal infusion of bradykinin elicits a pressor response in conscious rats via a B2-receptor mechanism

1999 ◽  
Vol 77 (8) ◽  
pp. 563-570 ◽  
Author(s):  
Kimberly M Hoagland ◽  
David A Maddox ◽  
Douglas S Martin
Keyword(s):  
Renal Artery ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Nerve Fibers ◽  
Maximum Response ◽  
Left Renal Artery ◽  
Response Curves ◽  
Afferent Nerve Fibers ◽  
Pressor Responses ◽  
Hoe 140

Bradykinin (BK) is a peptide known to activate afferent nerve fibers from the kidney and elicit reflex changes in the cardiovascular system. The present study was specifically designed to test the hypothesis that bradykinin B2 receptors mediated the pressor responses elicited during intrarenal bradykinin administration. Pulsed Doppler flow probes were positioned around the left renal artery to measure renal blood flow (RBF). A catheter, to permit selective intrarenal administration of BK, was advanced into the proximal left renal artery. The femoral artery was cannulated to measure mean arterial pressure (MAP). MAP, heart rate (HR), and RBF were recorded from conscious unrestrained rats while five-point cumulative dose-response curves during an intrarenal infusion of BK (5-80 µg·kg-1·min-1) were constructed. Intrarenal infusion of BK elicited dose-dependent increases in MAP (maximum pressor response, 26 ± 3 mmHg), accompanied by a significant tachycardia (130 ± 18 beats/min) and a 28% increase in RBF. Ganglionic blockade abolished the BK-induced increases in MAP (maximum response, -6 ± 5 mmHg), HR (maximum response 31 ± 14 beats/min), and RBF (maximum response, 7 ± 2%). Selective intrarenal B2-receptor blockade with HOE-140 (50 µg/kg intrarenal bolus) abolished the increases in MAP and HR observed during intrarenal infusion of BK (maximum MAP response, -2 ± 3 mmHg; maximum HR response, 15 ± 11 beats/min). Similarly, the increases in RBF were prevented after HOE-140 treatment. In fact, after HOE-140, intrarenal BK produced a significant decrease in RBF (22%) at the highest dose of BK. Results from this study show that the cardiovascular responses elicited by intrarenal BK are mediated predominantly via a B2-receptor mechanism.Key words: bradykinin, blood pressure, renal hemodynamics, B2 receptors, autonomic nervous system.

Regional hemodynamic and baroreflex effects of endothelin in rats

1989 ◽  
Vol 257 (3) ◽  
pp. H918-H926 ◽  
Author(s):  
M. M. Knuepfer ◽  
S. P. Han ◽  
A. J. Trapani ◽  
K. F. Fok ◽  
T. C. Westfall
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Nerve Activity ◽  
Anesthetized Rats ◽  
Pressor Responses ◽  
Regional Hemodynamics ◽  
Potent Vasoconstrictor ◽  
Baroreceptor Reflex Control

Endothelin is a peptide with potent, long-lasting pressor effects characterized by increases in mesenteric and hindquarters vascular resistance and bradycardia following an initial, transient depressor response. This study examined the mechanisms of action of endothelin on regional hemodynamics in conscious, freely moving rats and on baroreflex sensitivity both in conscious and chloralose-anesthetized rats. The pressor response to endothelin (0.67 nmol/kg) was attenuated by nifedipine (25 micrograms/kg) and augmented by chloralose anesthesia. The bradycardia was attenuated by pentolinium (10 mg/kg), atropine methyl sulfate (0.5 mg/kg), or chloralose anesthesia. Hindquarter vaso-constriction was attenuated by nifedipine, pentolinium, and atropine, whereas mesenteric vasoconstriction was less sensitive to blockade. The vasopressin V1 antagonist, [d(CH2)5Tyr(Me)]-AVP (20 micrograms/kg), indomethacin (5 mg/kg), or verapamil (150 micrograms/kg) did not affect any of these cardiovascular responses. Renal sympathetic nerve activity was reduced similarly in chloralose-anesthetized rats to pressor responses elicited by either phenylephrine or endothelin, and the slope of the baro-reflex function curve after endothelin was similar to that of phenylephrine. These results suggest that endothelin is a potent vasoconstrictor in which its action on visceral and skeletal muscle vasculature is mediated by somewhat different mechanisms. Endothelin does not alter baroreceptor reflex control of sympathetic nerve activity or heart rate.

Central effects of angiotensins I and II in conscious streptozotocin-treated rats

1990 ◽  
Vol 258 (5) ◽  
pp. R1147-R1156 ◽  
Author(s):  
K. C. Tomlinson ◽  
S. M. Gardiner ◽  
T. Bennett
Keyword(s):  
Pressor Response ◽  
Cardiovascular Responses ◽  
Brattleboro Rats ◽  
Ang Ii ◽  
Angiotensin I ◽  
Enhanced Sensitivity ◽  
Drinking Response ◽  
Pressor Responses ◽  
Long Evans ◽  
Residual Response

Responses to intracerebroventricular (icv) angiotensin II (ANG II) were measured in Long-Evans rats treated with the diabetogenic agent, streptozotocin (STZ), or saline 28 days earlier. STZ-treated Long-Evans rats showed normal pressor responses to ANG II in the absence of drinking water, but bradycardic responses were impaired although there was no reduction in baroreflex sensitivity. When allowed to drink, saline-treated, but not STZ-treated, rats showed an enhanced pressor response to icv ANG II and a tachycardia. Peripheral V1-receptor antagonism attenuated the pressor response to icv ANG II, leaving a residual response that was greater in saline-treated than in STZ-treated rats. STZ-treated rats had attenuated pressor and heart rate responses to icv angiotensin I (ANG I). Although some cardiovascular responses to icv ANG I and ANG II were reduced in STZ-treated rats, these animals showed enhanced sensitivity to the dipsogenic effects of the peptides. Vasopressin-deficient Brattleboro rats showed little pressor response to icv ANG II unless drinking was allowed, in which case the pressor response was less in STZ-treated than in saline-treated Brattleboro rats, although there was no difference in drinking response.

Inhibition of aortic chemoreceptor discharge by pressor response to muscular contraction

1987 ◽  
Vol 62 (6) ◽  
pp. 2258-2263
Author(s):  
K. W. McCoy ◽  
D. M. Rotto ◽  
M. P. Kaufman
Keyword(s):  
Arterial Pressure ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Muscular Contraction ◽  
Pressure Response ◽  
Hindlimb Muscles ◽  
Pressor Responses ◽  
Adrenergic Antagonist ◽  
Static Contraction

We have examined the effect of static contraction of the hindlimb muscles on the discharge of aortic chemoreceptors in chloralose-anesthetized cats. The responses of the chemoreceptors to contraction were dependent on the arterial pressure response to this maneuver. When contraction reflexly evoked a pressor response of at least 20 mmHg, the discharge of 26 chemoreceptors was reduced from control levels by 53% (P less than 0.01). The contraction-induced inhibition of chemoreceptor discharge was prevented by phentolamine, an alpha-adrenergic antagonist that also attenuated the contraction-induced pressor response. In addition, the inhibition evoked by contraction was simulated by injection of phenylephrine and inflation of an aortic balloon, both of which evoked pressor responses. However, when contraction failed to significantly change arterial pressure, the discharge of 20 aortic chemoreceptors was not significantly changed from control levels. We conclude that the reflex pressor response to static contraction inhibits the discharge of aortic chemoreceptors. This inhibition of discharge needs to be considered when interpreting the effects of aortic barodenervation on the cardiovascular responses to exercise.

Pressor responses of rats to vasopressin: effect of sodium, angiotensin, and catecholamines

1983 ◽  
Vol 244 (2) ◽  
pp. H253-H258 ◽  
Author(s):  
M. Burnier ◽  
H. R. Brunner
Keyword(s):  
Angiotensin Ii ◽  
Sodium Intake ◽  
Pressor Response ◽  
Response Curves ◽  
Ether Anesthesia ◽  
Spontaneously Hypertensive ◽  
Lysine Vasopressin ◽  
Pressor Responses ◽  
Wistar Kyoto ◽  
The Right

The pressor response to lysine vasopressin was tested in groups of male Wistar, Brattleboro, Wistar-Kyoto, and spontaneously hypertensive rats. Moreover, the influence of sodium intake, angiotensin II, saralasin, captopril, norepinephrine, and isoproterenol on vasopressin pressor responses was evaluated. The right iliac artery and one or both femoral veins of the animals were catheterized under light ether anesthesia. The experiments were carried out following a 2-h stabilization period with the rats awake and semirestrained. Pressor responsiveness was evaluated acutely on the basis of dose-response curves (0.5-4 mU). In the Wistar rats, angiotensin II (10 and 30 ng/min) and isoproterenol (10 ng/min) markedly decreased the response to vasopressin, whereas variations in sodium intake and blood pressure per se did not seem to exert any influence. Norepinephrine (250 ng/min) slightly enhanced the pressor responsiveness to the smaller doses of lysine-vasopressin. Brattleboro rats with congenital diabetes insipidus were less sensitive to vasopressin than the other animals, and neither angiotensin II nor isoproterenol induced any change. In conclusion, the pressor responsiveness to vasopressin can vary considerably depending on several factors. These must be taken into account when evaluating the possible pressor role of vasopressin in experimental and clinical settings.

Pressor Responsiveness to Angiotensin in Renovascular and Steroid Hypertension

1979 ◽  
Vol 57 (s5) ◽  
pp. 47s-50s ◽  
Author(s):  
E. S. Marks ◽  
H. Thurston ◽  
R. F. Bing ◽  
J. D. Swales
Keyword(s):  
Angiotensin Ii ◽  
Pressor Response ◽  
Plasma Renin ◽  
Receptor Occupancy ◽  
Bilateral Nephrectomy ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Pressor Responses ◽  
Salt Hypertension ◽  
Converting Enzyme Inhibition

1. The pressor response to angiotensin II was reduced in rats with early (<6 weeks) and chronic (>4 months) Goldblatt two-kidney, one-clip hypertension and enhanced in DOCA—salt hypertension. 2. Converting enzyme inhibition with captopril brought the angiotensin pressor response curves into closer proximity although the DOCA hypertensive rats were minimally hyper-responsive and rats with early and chronic renovascular hypertension showed slightly reduced responsiveness. 3. After bilateral nephrectomy the pressor responses to angiotensin were similar. 4. The pressor response to angiotensin II in these animals was inversely related to plasma renin concentration and therefore largely dependent upon receptor occupancy by endogenous angiotensin II. There is no evidence for enhanced pressor responsiveness to angiotensin in either renovascular or DOCA hypertension.

Stimulating fastigial nucleus pressor region elicits patterned respiratory responses

1986 ◽  
Vol 250 (3) ◽  
pp. R418-R426 ◽  
Author(s):  
L. O. Lutherer ◽  
J. L. Williams
Keyword(s):  
Respiratory Rate ◽  
Active Sites ◽  
Pressor Response ◽  
Stimulus Frequency ◽  
Cardiovascular Responses ◽  
Fastigial Nucleus ◽  
Response Curves ◽  
Low Frequencies ◽  
Phase Switching ◽  
Respiratory Responses

Electrical stimulation of the ventromedial region of the rostral fastigial nucleus (FN) in the cat produced marked quantifiable changes in respiration that were highly correlated with the concurrently elicited cardiovascular responses. The threshold- and stimulus-response curves were very similar for the two responses. Stimulation at relatively low frequencies produced increases in respiratory rate at all active sites. At approximately half the sites biphasic responses were observed with increases in stimulus frequency. These were characterized by a transient period of apnea beginning with onset of the stimulus, followed by an increased respiratory rate. At the remaining sites respiratory rate increased at all stimulation frequencies tested. Inspiratory duration decreased, and mean inspiratory flow increased. Tidal volume was not significantly altered. Similar changes were also observed when the pressor response was blocked by phenoxybenzamine. These observations, together with the frequent demonstration of expiratory-to-inspiratory and inspiratory-to-expiratory phase switching with short-burst stimulation, suggest that the FN can influence a respiratory central pattern generator. Based on these findings, a possible role for the FN in integrating cardiovascular and respiratory responses is suggested.

Fluid volumes and pressor responsiveness in two-kidney rabbits with renal artery stenosis

1982 ◽  
Vol 243 (5) ◽  
pp. H779-H787 ◽  
Author(s):  
J. A. Johnson ◽  
K. D. Kurz ◽  
S. Siripaisarnpipat ◽  
D. W. Zeigler ◽  
C. G. Payne
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Body Fluid ◽  
Cardiovascular Responses ◽  
Artery Stenosis ◽  
Control Group ◽  
Ang Ii ◽  
Pressor Responses

This study examined body fluid volumes, the pressor responses to norepinephrine (NE), and the cardiovascular responses to NE before and during infusion of an angiotensin II (ANG II) antagonist in two-kidney rabbits with unilateral renal artery stenosis (RAS) of 3 and 30 day duration. Three separate experiments were performed. In the first experiment, plasma volume, extracellular fluid volume, and total body water were measured by the distribution volumes of radioiodinated serum albumin, 35SO4, and tritiated water, respectively. No differences were seen for any of these volumes between the 3- or 30-day RAS rabbits and their controls. In the second experiment, pressor responses to infusions of several doses of NE were examined; rabbits with 3- and 30-day RAS had exaggerated pressor responses to all doses of NE when compared with the control rabbits. In the third experiment, infusion of NE at 800 ng.min-1.kg body wt-1 resulted in more pronounced increases in mean arterial pressure and total peripheral resistance (TPR) in the 3- and 30-day RAS rabbits than in the controls; after infusion of [Sar1-Ile8] ANG II the increases in mean arterial pressure and TPR during NE infusion were blunted and were of the same magnitude as in the control group. In all experiments the 30-day RAS rabbits were hypertensive, whereas the 3-day RAS rabbits were normotensive; also, plasma renin activity (PRA) values were normal in both the 3- and 30-day RAS groups. These studies demonstrated that increases in body fluid volumes are not necessary for pressor and vascular hyperresponsiveness probably is mediated by ANG II, despite normal PRA values.

Disappearance of Angiotensin II and Noradrenaline from the Renal and Femoral Circulations of the Dog

1980 ◽  
Vol 58 (1) ◽  
pp. 29-35 ◽  
Author(s):  
M. J. S. Miller ◽  
G. C. Scroop
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Femoral Artery ◽  
Pressor Response ◽  
Intravenous Route ◽  
Vascular Bed ◽  
Pressor Responses ◽  
Vascular Beds ◽  
Degree Of Extraction ◽  
Renal Vascular

1. The relative ability of the renal and femoral vascular beds to remove infused angiotensin II and noradrenaline was examined in anaesthetized greyhounds. 2. The degree of extraction of infused drug by each vascular bed was expressed as a percentage, calculated by comparing the pressor response to intra-arterial infusion with that obtained when the same dose was administered by the intravenous route. 3. When compared with the same dose given intravenously, the pressor responses after renal artery administration of angiotensin II were reduced by a mean of 77·8 ± 4·1% (mean ± sem, n = 12), whereas those after femoral artery infusions at the same dose were reduced by a mean of only 27·2 ± 4·9%(n = 12). 4. The pattern of extraction seen with noradrenaline infusions administered in a similar manner was the reverse of that with angiotensin II. There was a 28·9 ± 6·8% (n = 7) reduction in pressor responses to renal artery infusions; in contrast, femoral artery infusions of the same dose exhibited a 99·0 ± 1·0% (n = 7) reduction in the pressor responses. 5. Local arterial administration of the angiotensin II competitive antagonist, [Sar1,Ile8]angiotensin II, potentiated the systemic pressor responses to renal artery infusions of angiotensin II, but not those to femoral artery infusions. 6. It is suggested that the marked ability of the renal vascular bed to remove circulating angiotensin II may, in part, involve receptor-binding, although this seems not to be the case in the femoral vascular bed.

Bradykinin BK2 receptors contribute to reflex cardiovascular responses during brief abdominal ischemia

1998 ◽  
Vol 274 (1) ◽  
pp. H308-H313 ◽  
Author(s):  
Premjit S. Chahal ◽  
Stephen V. Rendig ◽  
John C. Longhurst
Keyword(s):  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Nerve Fibers ◽  
Reflex Response ◽  
Receptor Antagonists ◽  
Artery Ligation ◽  
Sympathetic Nerve Fibers ◽  
Arterial Blood ◽  
Afferent Nerves ◽  
Hoe 140

Ischemically sensitive visceral sympathetic nerve fibers, which are thought to represent the afferent limb of a strong cardiovascular pressor reflex, can be stimulated by exogenously applied bradykinin (BK). During ischemia, BK also is known to be produced locally and to serve as an endogenous stimulus for activation of ischemically sensitive nerve endings. It is unclear, however, whether ischemically induced BK production is sufficient to elicit a reflex cardiovascular response. Accordingly, femoral arterial and venous catheters were positioned in anesthetized cats, and the superior mesenteric and celiac arteries were isolated for placement of snare occluders. After dual occlusion of these arteries (20 min), one of two chemically dissimilar specific kinin B2(BK2) receptor antagonists, HOE-140 (30–40 μg/kg iv, n = 8) or NPC-17731 (30–40 μg/kg iv, n= 11), was administered and dual occlusion was repeated. The reflex rise of mean arterial blood pressure (BP) of 16 ± 3.7% was significantly ( P < 0.05) reduced by HOE-140 to 8.4 ± 2.0%. NPC-17731 similarly attenuated the reflex BP increment from 13 ± 1.2 to 6.2 ± 1.6% ( P < 0.05). In a separate set of control animals the first and second periods of ischemia induced reflex BP increments that did not differ significantly (16 ± 2.7 and 16 ± 5.7%, respectively). Qualitatively similar decrements of the BP response were produced by the BK2 receptor antagonists in two additional groups in which blood flow to the superior mesenteric and celiac arteries was diverted to a venous reservoir to eliminate the initial transient (mechanically induced) rise in BP associated with artery ligation that is known not to be associated with the reflex response. These results indicate that the stimulation of BK2 receptors on visceral afferent nerves by BK is responsible, at least in part, for the reflex cardiovascular response during visceral ischemia.

Pressor responses to vasopressin in rabbits with 3-day renal artery stenosis

1981 ◽  
Vol 240 (6) ◽  
pp. H862-H867 ◽  
Author(s):  
J. A. Johnson ◽  
S. Ichikawa ◽  
K. D. Kurz ◽  
W. L. Fowler ◽  
C. G. Payne
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Cardiovascular Responses ◽  
Artery Stenosis ◽  
Vasopressin Infusion ◽  
Pressor Responses

One-kidney rabbits were subjected to renal artery stenosis, and acute experiments were performed 3 days later on conscious animals; one-kidney rabbits without renal artery stenosis served as controls. Rabbits with 3-day renal artery stenosis were normotensive and had normal values for plasma renin activity. Intravenous infusion of arginine vasopressin at 5 mU.min-1.kg body wt-1 for 5 min resulted in a significantly (P less than 0.01) greater increase in mean arterial pressure and total peripheral resistance (TPR) in the renal artery stenosis rabbits than in the controls. Infusion of the angiotensin II (AII) competitive antagonist, [Sar1, Ile8]AII, before the vasopressin infusion abolished the hyperresponsiveness to vasopressin in the renal artery stenosis rabbits and resulted in changes in mean arterial pressure and TPR that were approximately of the same magnitude as the controls. Infusion of [SAr1, Ile8]AII before vasopressin infusion in control rabbits did not alter the cardiovascular responses to vasopressin. Because previous studies have shown that 3-day renal artery stenosis rabbits have exaggerated pressor responses to norepinephrine and that this hyperresponsiveness to norepinephrine is blocked by [Sar1, Ile8]-AII, the present study with vasopressin provided evidence that the increased responsiveness in this model is not specific for a single pressor agent. These studies also demonstrated that AII plays an important role in mediating the exaggerated pressor responses to vasopressin in this prehypertensive model.

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