Comparison of fast and slow pressor effects of angiotensin II in the conscious rat

Brown, Anthony R.; Casals-Stenzel, J.; Gofford, S.; Lever, A. F.; Morton, J. J.

doi:10.1152/ajpheart.1981.241.3.h381

Cited by 67 publications

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“…Based on our data showing that hematocrit was not different, it seems unlikely that an increase in ECF volume occurred in our model. This result appears consistent with those of other studies showing no change in sodium and water balance or ECF volume in animals chronically infused with ANG II (7,18). Overall, the conclusion that chronic ANG II infusion did not significantly affect ongoing atrial compliance is supported by evidence that MRAP responses during VE did not differ between animals that received chronic ANG II compared with those infused with vehicle alone.…”

Section: Discussionsupporting

confidence: 91%

Chronic angiotensin II infusion attenuates the renal sympathoinhibitory response to acute volume expansion

LaGrange

Toney

Bishop

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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In this study the hypothesis was tested that chronic infusion of ANG II attenuates acute volume expansion (VE)-induced inhibition of renal sympathetic nerve activity (SNA). Rats received intravenous infusion of either vehicle or ANG II (12 ng·kg −1 ·min −1 ) for 7 days. ANG II-infused animals displayed an increased contribution of SNA to the maintenance of mean arterial pressure (MAP) as indicated by ganglionic blockade, which produced a significantly (P < 0.01) greater decrease in MAP (75 ± 3 mmHg) than was observed in vehicle-infused (47 ± 8 mmHg) controls. Rats were then anesthetized, and changes in MAP, mean right atrial pressure (MRAP), heart rate (HR), and renal SNA were recorded in response to right atrial infusion of isotonic saline (20% estimated blood volume in 5 min). Baseline MAP, HR, and hematocrit were not different between groups. Likewise, MAP was unchanged by acute VE in vehicle-infused animals, whereas VE induced a significant bradycardia (P < 0.05) and increase in MRAP (P < 0.05). MAP, MRAP, and HR responses to VE were not statistically different between animals infused with vehicle vs. ANG II. In contrast, VE significantly (P < 0.001) reduced renal SNA by 33.5 ± 8% in vehicle-infused animals but was without effect on renal SNA in those infused chronically with ANG II. Acutely administered losartan (3 mg/kg iv) restored VEinduced inhibition of renal SNA (P < 0.001) in rats chronically infused with ANG II. In contrast, this treatment had no effect in the vehicle-infused group. Therefore, it appears that chronic infusion of ANG II can attenuate VE-induced renal sympathoinhibition through a mechanism requiring AT 1 receptor activation. The attenuated sympathoinhibitory response to VE in ANG II-infused animals remained after arterial barodenervation and systemic vasopressin V 1 receptor antagonism and appeared to depend on ANG II being chronically increased because ANG II given acutely had no effect on VE-induced renal sympathoinhibition. Keywordssympathetic nerve activity; cardiopulmonary reflex; body fluid balance; arterial baroreceptor reflex Numerous studies have investigated interactions between circulating ANG II and the arterial baroreceptor reflex. Whereas recent studies indicate that an acute increase in circulating ANG II can attenuate the increase in sympathetic nerve activity (SNA) that follows arterial baroreceptor unloading (34), chronic increases of ANG II have been repeatedly demonstrated to reset arterial baroreflex control of SNA (4, 6). The latter effect may permit SNA to rise relative to the prevailing level of arterial pressure. In addition to the arterial Copyright © 2003 NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript baroreflex, the cardiopulmonary baroreflex is also an important determinant of sympathetic outflow as well as sodium and water balance. However, the extent to which chronic increases of ANG II might interact with this reflex to modify the SNA response to volume expansion (VE) is not known. This is surprising given that norma...

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Section: Discussionsupporting

confidence: 91%

Chronic angiotensin II infusion attenuates the renal sympathoinhibitory response to acute volume expansion

LaGrange

Toney

Bishop

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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“…[1][2] This hypertensive response, known as the slow pressor response to Ang II, has been shown by many laboratories including our own. 3 Most have studied this phenomenon using tail cuff plethysmography (TCP) to measure blood pressure in the conscious animals.…”

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confidence: 61%

Low-Dose Angiotensin II Enhances Pressor Responses Without Causing Sustained Hypertension

et al. 2003

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Abstract-Subpressor doses of angiotensin II (SP-Ang II) cause a slow increase in blood pressure in rats as assessed by tail cuff plethysmography (TCP), reflecting either sustained hypertension or an exaggerated pressor response to diverse stimuli. We examined whether subpressor doses of Ang II enhance blood pressure responses to simple stress (handling of trained rats for TCP). We implanted telemetry in Sprague-Dawley rats. After 10 days of recovery and TCP training, we implanted osmotic minipumps with either SP-Ang II (50 ng/kg per minute) or vehicle, and then measured systolic blood pressure continuously in unrestrained rats for 13 days. We also recorded telemetry readings while obtaining TCP measurements every 2 days. SP-Ang II increased blood pressure from 134Ϯ19 to 159Ϯ22 mm Hg by TCP, which matched the simultaneous telemetry readings of 131Ϯ20 to 154Ϯ25 mm Hg. In contrast, SP-Ang II did not change the blood pressure in the unrestrained rats (measured with continuous telemetry: 124Ϯ2 versus 127Ϯ1 mm Hg). The blood pressure in the control rats did not change in the unrestrained state (125Ϯ3 versus 128Ϯ5 mm Hg on days 0 and 12, respectively), and only slightly increased during TCP (11Ϯ5 and 6Ϯ4 mm Hg by TCP and simultaneous telemetry, respectively; PϭNS). In summary, SP-Ang II, although unable to provoke sustained hypertension, nonetheless magnifies the pressor response to otherwise trivial stimuli. We speculate that even modestly elevated Ang II levels may contribute to hypertensive complications because such levels promote the punctuation of an apparent normotensive state by episodic hypertension occasioned by seemingly innocuous stimuli. Key Words: angiotensin II, Ⅲ hypertension, experimental Ⅲ blood pressure Ⅲ vasculature C hronically infusing a subpressor dose of angiotensin II (SP-Ang II) increases blood pressure after several days. 1-2 This hypertensive response, known as the slow pressor response to Ang II, has been shown by many laboratories including our own. 3 Most have studied this phenomenon using tail cuff plethysmography (TCP) to measure blood pressure in the conscious animals. 1,2,3 Although this technique is very valuable, it does have certain limitations. For instance, it does not allow for continuous monitoring of blood pressure. In addition, the procedure is somewhat cumbersome and involves warming the rats, placing them in restraining cages, and then inflating the tail cuff; all of these steps have been shown to induce a stress response in trained normotensive animals, which consequently may alter the blood pressure. 4,5 Recently, a radiotelemetric recording system has been developed, which permits long-term continuous monitoring of blood pressure in animals without the stress of heating, handling, or restraining. 6,7 Thus, we incorporated this new technology in our laboratory to enhance our blood pressure monitoring during SP-Ang II-induced hypertension (HTN). Using this methodology, we initially attempted to reproduce our previous findings. However, we were surprised to find that 5 ng/k...

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“…The angiotensin II (AngII) slow pressor response is a gradually developing increase in BP (BP) with an initially subpressor rate of infusion (1)(2)(3)(4). The slow pressor response was first described in rats in 1963, (1) and subsequently has been demonstrated in rabbits, dogs and man (5).…”

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confidence: 99%

A Mouse Model of Angiotensin II Slow Pressor Response

Kawada

Imai

Karber³

et al. 2002

Journal of the American Society of Nephrology

182

183

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Abstract. The slow pressor response to prolonged infusions of angiotensin II (AngII) entails a delayed rise in BP. This study investigated the hypothesis that the response depends on the generation of oxidative stress. The BP and renal functional response of mice to graded doses (200, 400, and 1000 ng · kg Ϫ1 · min Ϫ1 ) of subcutaneously infused AngII was studied. The SBP of conscious mice increased by day 3 at AngII1000 but showed a delayed rise by days 9 to 13 (slow pressor response) at the lower rates of AngII infusion. By day 13, there was a graded increase in SBP with the rate of AngII infusion (Vehicle, Ϫ2.6 Ϯ 2.6%; AngII200, ϩ14.1 Ϯ 5.0%; AngII400, ϩ31.9 Ϯ 1.9%; AngII1000, ϩ43.2 Ϯ 5.5%). The MAP measured under anesthesia rose significantly (P Ͻ 0.001) with AngII400 at 14 d (Vehicle, 85 Ϯ 2 mmHg; AngII400, 100 Ϯ 3 mmHg). When studied at day 6, the MAP of AngII400 rats was not elevated (88 Ϯ 2 mmHg; NS versus vehicle), yet the GFR was higher (1.05 Ϯ 0.05 versus 1.25 Ϯ 0.05 ml · min Ϫ1 · g Ϫ1 ; P Ͻ 0.05) accompanied by an increase in the filtration fraction (FF) (28.8 Ϯ 1.2 versus 37.2 Ϯ 0.8%; P Ͻ 0.001). From day 6 through day 14, the MAP had increased (P Ͻ 0.01) in AngII400, accompanied by a significant reduction in GFR to 1.05 Ϯ 0.04 ml · min Ϫ1 · g Ϫ1 (P Ͻ 0.01) and elevation of renal vascular resistance (RVR) (day 6 versus day 14, 15.3 Ϯ 0.6 versus 19.2 Ϯ 1.2 mmHg · ml Ϫ1 · min Ϫ1 · g Ϫ1 ; P Ͻ 0.05). Renal excretion of 8-iso PGF 2␣ was increased in AngII400 group at day 12 (2.52 Ϯ 0.35 versus 5.85 Ϯ 0.78 pg · day Ϫ1 ; P Ͻ 0.01). The permeant superoxide dismutase mimetic tempol reduced the effects of AngII400 on the SBP (Ϫ1.7 Ϯ 5.8%; P Ͻ 0.01), the MAP (87 Ϯ 4 mmHg; P Ͻ 0.01), and the RVR (15.2 Ϯ 0.5 mmHg · ml Ϫ1 · min Ϫ1 · g Ϫ1 ; P Ͻ 0.05) at day 14 and the renal 8-iso PGF 2␣ excretion (3.53 Ϯ 0.71 pg · d Ϫ1 ; P Ͻ 0.05) at day 12. It is concluded that the AngII infused mouse is a valid model for the slow pressor response. There is an early rise in GFR and FF, consistent with increased postglomerular vascular resistance and a late rise in RVR with a fall in GFR, consistent with increased preglomerular vascular resistance that is accompanied by a rise in BP. There is evidence of increased oxidative stress that is implicated in the increase in the BP and RVR in this model.The angiotensin II (AngII) slow pressor response is a gradually developing increase in BP (BP) with an initially subpressor rate of infusion (1-4). The slow pressor response was first described in rats in 1963, (1) and subsequently has been demonstrated in rabbits, dogs and man (5). Whereas the plasma AngII levels increase by about 80-fold during an immediate pressor response, they are elevated within a physiologic level of 2-to sixfold during a slow pressor response (6). A slow pressor response is seen also with the thromboxane A2/prostaglandin H2 (TP) receptor mimetic, U-46619 (7,8). This slow pressor response has been considered an excellent model for renal hypertension in which both AngII type I (AT1) and TP receptor have been implica...

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Comparison of fast and slow pressor effects of angiotensin II in the conscious rat

Cited by 67 publications

References 0 publications

Chronic angiotensin II infusion attenuates the renal sympathoinhibitory response to acute volume expansion

Chronic angiotensin II infusion attenuates the renal sympathoinhibitory response to acute volume expansion

Low-Dose Angiotensin II Enhances Pressor Responses Without Causing Sustained Hypertension

A Mouse Model of Angiotensin II Slow Pressor Response

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