Arterial Baroreceptor Resetting: Contributions of Chronic and Acute Processes

Andresen, Michael; Yang, Mingyong

doi:10.1111/j.1440-1681.1989.tb02993.x

Cited by 75 publications

(50 citation statements)

References 21 publications

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“…In spontaneously hypertensive rats (SHR), resetting of the baroreceptor with depressed sensitivity is observed. 2 We have demonstrated that exercise training improves both the depressed baroreflex control of heart rate and reduces the level of arterial hypertension in SHR. After a 12-week period of low-intensity exercise training, the baroreflex sensitivity to bradycardia and tachycardia returned to near-normal values.…”

mentioning

confidence: 90%

Exercise Training Increases Baroreceptor Gain Sensitivity in Normal and Hypertensive Rats

et al. 2000

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Abstract-Exercise training attenuates arterial hypertension and increases baroreflex sensitivity in spontaneous hypertension. However, no information exists regarding the portion of the baroreflex arch in which this attenuation takes place. We tested the hypothesis that exercise training increases the afferent pathway sensitivity of baroreflex control in both normotensive and spontaneously hypertensive rats (SHR). Arterial pressure and whole-nerve activity of the aortic baroreceptor (multifiber preparation) were evaluated in 30 male rats assigned to 4 groups: sedentary and exercise-trained normotensive rats and sedentary and exercise-trained SHR. Exercise training was performed on a motor treadmill, 5 d/wk for 60 minutes, gradually progressing toward a speed of 26.8 m/min. Exercise training reduced mean arterial pressure in conscious exercise-trained SHR (183Ϯ4 versus 165Ϯ7 mm Hg). The relation between changes in aortic baroreceptor discharge and changes in systolic arterial pressure increased significantly in exercise-trained normotensive rats (2.09Ϯ0.1 versus 1.44Ϯ0.1%/mm Hg) and exercise-trained SHR (0.92Ϯ0.1 versus 0.71Ϯ0.1%/mm Hg) compared with their respective sedentary rats. Likewise, the average aortic baroreceptor gain sensitivity (calculated by logistic equation) was significantly higher in exercise-trained normotensive rats (2.25Ϯ0.19 versus 1.77Ϯ0.03%/mm Hg) and exercise-trained SHR (1.07Ϯ0.04 versus 0.82Ϯ0.05%/mm Hg) compared with their respective sedentary control rats. In conclusion, exercise training increases aortic baroreceptor gain sensitivity in normotensive and SHR, thus improving baroreceptor sensitivity, which may result in a more efficient arterial pressure regulation by the baroreflexes.

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confidence: 90%

Exercise Training Increases Baroreceptor Gain Sensitivity in Normal and Hypertensive Rats

et al. 2000

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“…1, inset). Since baroreceptors are actually activated by vessel wall stretch (Andresen & Yang, 1989 b), we also monitored the relation between aortic diameter and baroreceptor discharge (Fig. 2).…”

Section: Resultsmentioning

confidence: 99%

“…First, changes in smooth muscle tension, and therefore aortic diameter, evoke selective changes in threshold and therefore manifest themselves as parallel shifts of the pressure-response curve with no changes in threshold discharge frequency, suprathreshold gain, or maximal discharge rates . Second, changes in conditioning pressure (or diameter) selectively affect threshold and no other parameter of the discharge-response curve (Andresen & Yang, 1989 b). The mechanisms responsible for both rapid resetting and for smooth muscle modulation of baroreceptors are unknown, but they may be related .…”

Section: Discussionmentioning

confidence: 99%

Contrasting actions of cocaine, local anaesthetic and tetrodotoxin on discharge properties of rat aortic baroreceptors.

Andresen

Brodwick

Yang

1994

The Journal of Physiology

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1. Effects of cocaine, lignocaine, benzocaine and tetrodotoxin (ITX) on the simultaneously measured pressure-and diameter-discharge frequency relations of single fibre baroreceptors were compared in rat in vitro aortic arch-aortic nerve preparations.2. Between 1 and 10 /M, cocaine produced selective increases in the pressure threshold shifting the pressure-response curve without altering the gain or threshold frequency. At near-blocking concentrations, gain was depressed as well. Cocaine experiments were done in nitroprusside (NP, 1 ,C4M). Neither NP or NP with cocaine altered diameter (P > 0-36).3. Lignocaine (at >10 /sM) and benzocaine (at >100 /SM) shifted pressure-response curves to higher pressures and generally depressed discharge by increasing pressure threshold and decreasing maximum discharge frequency (P <0-05). Gain decreased and threshold frequency increased at higher concentrations. Diameter was unaffected by lignocaine or benzocaine (P > 0-14). 4. ITX increased thresholds and discharge frequencies at threshold but did not shift pressure-discharge curve locations. This produced superimposable discharge curves with changes occurring as losses of discharge points in the threshold region. Diameter was unaffected by TTX (P > 0 80). 5. The contrasting patterns of effects between [TX and local anaesthetics suggest that blockade of ITX-sensitive sodium channels alone may not be responsible for the effects of cocaine, lignocaine and benzocaine.Cocaine disrupts baroreceptor discharge in micromolar concentrations (Andresen, Yang, Nelson & Steinsland, 1990) which appear too low for conventional axonal blockade by local anaesthetic action (50 % block at about 400/uM; Gissen, Covino & Gregus, 1980 The aortic arch and aortic nerve were dissected free of surrounding tissues. These methods have previously been described in detail . Briefly, the innominate artery and descending aorta were cannulated with stainless-steel cannulae and the remaining vessels of the aortic arch were closed with ligatures. The arch and nerve were then removed and mounted in a temperature-regulated (36-37°C) perfusion dish, pinned to approximate the in situ configuration and covered with warmed mineral oil. The arch was continuously perfused (3 ml min') with a physiological buffered salt solution (PBS) continuously gassed with 95 % 02-5 % CO2.PBS contained the following (mM): NaCl, 120; KCl, 4'8; KH2P04, 1-2; MgSO4, 1.2; NaHCO3, 25; dextrose, 5'5; CaCl2, 11.To measure diameter, the aorta was positioned over a central MS 2677, pp. 309-319 309 M. C. Andresen, M. Brodwick and M. Yang glass window in the floor of the perfusion chamber and the shadow of the aorta was cast on the photodiode detector arrays of a custom-made, high-resolution (0-02% or 1jsm) photomicrometer (Munch, Iwazuni & Brown, 1985). The aortic diameter just distal to the left subelavian artery was measured continuously throughout all experiments.The aortic nerve was divided into fine strands containing a single active baroreceptor and differentially recorded using a pair o...

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“…10 In chronic hypertension, baroreceptor responsiveness to pressure is decreased: pressure threshold is increased and gain is decreased. These are the classic hallmarks of chronic hypertensive baroreceptor resetting.…”

Section: Rapid Resettingmentioning

confidence: 99%

“…4 Chronic adjustments in baroreceptor threshold and sensitivity occur during development, aging, and hypertension. 7 - 9 However, since rapid resetting is a quantitatively important determinant of baroreceptor threshold, 10 differences in the short-term adaptability of DS rat baroreceptors might contribute to the measured differences in baroreceptor properties. Although the mechanism of rapid resetting is not known, recent studies suggest that characteristics of Received June 25, 1990; accepted in revised form November 9, 1990. the baroreceptor itself and not vessel wall mechanical properties might be responsible.…”

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confidence: 99%

Rapid baroreceptor resetting in Dahl salt-sensitive rats.

Yang

Andresen

1991

Hypertension

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Dahl salt-sensitive rats rapidly become hypertensive when exposed to a high salt diet, but Dahl salt-resistant rats maintain normal blood pressure on a high salt diet A defect in baroreceptor afferents is thought to play a key role in the low sensitivity of baroreceptor reflexes in Dahl salt-sensitive rats even in the prehypertensive stage during low salt treatment In the present study, we tested whether differences in rapid resetting ability might contribute to differences in baroreceptor function in Dahl rats. Four groups of rats were tested: salt-sensitive and salt-resistant rats on low salt and high salt diets (0.15% and 8.0% NaCl). We compared the rapidly resetting responses of baroreceptors from each group using an in vitro preparation. Rapid resetting was assessed for each aortic baroreceptor (n=46) by linear fit of the relation of pressure threshold and conditioning mean arterial pressure. Each group had a wide range of resetting ratios (the slope of the resetting relation). Despite higher initial pressure thresholds in salt-sensitive rats on a high salt diet, resetting ratios among the four groups were similar. Thus, the ability of Dahl salt-sensitive baroreceptors to rapidly reset is preserved, despite high dietary salt and a genetic predisposition to dysfunction. The present findings in Dahl rats reinforce the results of recent studies of rapid resetting during spontaneous and renal hypertension, which suggests that the rapid resetting process is remarkably resistant to factors that compromise baroreceptor function. (Hypertension 1991;17:541-545)D an] salt-sensitive (DS) rats rapidly develop high blood pressure when exposed to a high salt diet, but Dahl salt-resistant (DR) rats maintain normal blood pressure on this diet.1 Baroreceptor reflex control of blood pressure is abnormal in DS rats even on a low salt diet. 2 -3 Aortic nerve recordings suggest that the function of arterial baroreceptor afferents is impaired in prehypertensive DS rats on a low salt diet. 4 -6 This afferent defect probably accounts for the low sensitivity of baroreceptor reflexes in DS rats during low salt treatment. 4 Chronic adjustments in baroreceptor threshold and sensitivity occur during development, aging, and hypertension. 7 -9 However, since rapid resetting is a quantitatively important determinant of baroreceptor threshold, 10 differences in the short-term adaptability of DS rat baroreceptors might contribute to the measured differences in baroreceptor properties. Although the mechanism of rapid resetting is not known, recent studies suggest that characteristics of the baroreceptor itself and not vessel wall mechanical properties might be responsible.11 " 16 If the baroreceptor defect in DS rats is genetic, it might affect the ability of baroreceptors to rapidly reset. The present study compares the ability of baroreceptors in DS and DR rats on high and low salt diets to rapidly reset. MethodsMale DR and DS rats were obtained from Harlan Sprague Dawley, Inc., Indianapolis, Ind., at 4 weeks of age. Each rat strain was d...

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Arterial Baroreceptor Resetting: Contributions of Chronic and Acute Processes

Cited by 75 publications

References 21 publications

Exercise Training Increases Baroreceptor Gain Sensitivity in Normal and Hypertensive Rats

Exercise Training Increases Baroreceptor Gain Sensitivity in Normal and Hypertensive Rats

Contrasting actions of cocaine, local anaesthetic and tetrodotoxin on discharge properties of rat aortic baroreceptors.

Rapid baroreceptor resetting in Dahl salt-sensitive rats.

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