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M C Andresen

Publications and source records attributed to M C Andresen.

At least 37 records · Page 2Linked to original sources
PubMed1992

Gadolinium and mechanotransduction of rat aortic baroreceptors.

The cellular mechanisms enabling baroreceptors to transduce wall distortion into axonal discharge are unknown but might involve stretch-activated ion channels. Gadolinium (Gd3+, 10 microM) blocks stretch-activated channels in several preparations. Here we tested Gd3+ effects on discharge responses of 15 single-fiber baroreceptors in vitro. We simultaneously measured discharge, pressure, and aortic diameter at Gd3+ concentrations from 0.001 to 400 microM. High levels of Gd3+ added to a bicarbonate-buffered perfusate (Krebs) slightly shifted the pressure-discharge relation (less than 4 mmHg, n = 3, P = 0.01) without affecting slope or discharge frequency at threshold. Gd3+ in Krebs variably altered the pressure-diameter relation. Because 500 microM Gd3+ produced visible precipitate in Krebs, we tested Gd3+ in a simpler perfusate using N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES). Gd3+ in HEPES (n = 10) induced minor, but statistically significant, average increases in threshold (less than +5-7%) and no changes in gain. However, prolonged HEPES exposure alone (n = 2) produced similar shifts. Electron microscopy verified that Gd3+ diffused from the lumen to reach extracellular locations near baroreceptor endings. We conclude that 1) HEPES perfusate alone reversibly depresses baroreceptor discharge and 2) Gd3+ has no direct effects on baroreceptors. Thus it appears that aortic baroreceptor mechanotransduction must utilize a different class of stretch-activated ion channels.

Animals↗
PubMed1992

Smooth muscle tone and rapid resetting of rat aortic baroreceptors.

Changes in conditioning mean arterial pressure (cMAP) selectively alter the set point of arterial baroreceptors and baroreflexes without affecting gain. Changes in smooth muscle tone at constant cMAPs shift the pressure-discharge curves of aortic baroreceptors in a similar manner. Using an in vitro preparation of the rat aortic arch, we tested whether near maximal changes in smooth muscle tone affect rapid resetting in single regularly discharging aortic baroreceptors. Discharge, pressure, and aortic diameter were simultaneously measured. By using vasoactive drugs (phenylephrine, angiotensin II, Bay K 8644, and nitroprusside), rapid resetting to cMAP changes was tested during different smooth muscle tone conditions (control, constricted, and dilated). Baroreceptor discharge-response curves were periodically assessed with slow ramps of increasing pressure at each of three different cMAP levels (10-15 minutes each). Rapid resetting relations were constructed for pressure threshold (Pth) and diameter threshold (Dth) plotted against cMAP and conditioning diameter (cD), respectively. Vasoconstriction decreased Pth in all baroreceptors (n = 13, p less than 0.05). Baroreceptor resetting ability as indicated by the slopes of the resetting relations (pressure- or diameter-resetting ratios, delta Pth/delta cMAP or delta Dth/delta cD, respectively) was unaffected by large increases in smooth muscle tone (p greater than 0.12). Vasoconstriction, however, offset the pressure-resetting relation, shifting the linear relation in a parallel manner to higher Pth values. In contrast, Dth values during vasoconstriction were not offset but instead fell along a single diameter-resetting relation coincident with the control relation for each baroreceptor. This last result suggests that acute alteration of vessel mechanics by vasoconstriction does not alter the basic rapid resetting process.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Rapid baroreceptor resetting in Dahl salt-sensitive rats.

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.

Animals↗
PubMed1990

Cocaine inhibits baroreflex control of blood pressure by actions at arterial baroreceptors.

Blood pressure and heart rate often increase during cocaine intoxication, but the mechanisms of these cardiovascular responses are poorly understood. The most often suggested theories are central nervous system mechanisms involving the blockade of neuronal transmitter uptake. Cocaine also has potent local anesthetic properties, and in this study we tested the possible role of peripheral actions of cocaine at baroreceptor afferents. Single fiber baroreceptors were recorded using an in vitro preparation of the rat aortic arch. Diameter, pressure, and baroreceptor discharge were recorded. Cocaine perfused through the lumen of the aortic arch at a suprathreshold pressure reduced baroreceptor discharge within 90 s of entering the lumen of the aorta. Slow ramps of pressure elicited complete pressure- and diameter-discharge curves every 5 min. Beginning at about 1 microM, cocaine inhibited baroreceptor function; threshold increased, the maximum discharge decreased, and at 100 microM cocaine, all discharge ceased. The vasodilator nitroprusside or the alpha 1-adrenoreceptor antagonist prazosin did not affect baroreceptor responses to cocaine. In in vivo tests in rabbits, cocaine that perfused through a vascularly isolated carotid sinus reduced the slope of the baroreflex relationship between carotid sinus pressure and systemic mean arterial pressure. Significant depression of baroreceptor function was found at concentrations similar to the plasma cocaine levels measured in clinical studies. The local anesthetic properties of cocaine may be involved in baroreceptor effects. Our studies suggest a possible contributing role of a new site of action of cocaine outside the central nervous system. Compromise of baroreceptor reflexes could facilitate the development of serious cardiovascular complications associated with cocaine abuse.

Animals↗
PubMed1990

Non-NMDA receptors mediate sensory afferent synaptic transmission in medial nucleus tractus solitarius.

Indirect evidence suggests that excitatory amino acids (EAA) are involved in synaptic transmission of visceral afferents at their synapses within the nucleus tractus solitarius (NTS). Little is known about the identity of the postsynaptic receptors or response mechanisms. Here we report results from a longitudinal brain slice of the rat medulla. Intracellular recordings were made from neurons in delimited portions of the dorsal medial NTS (mNTS) known to receive baroreceptor inputs. Stimulation of the solitary tract 1-3 mm from the mNTS recording site evoked short (2 ms) latency excitatory postsynaptic potentials (EPSPs), which had durations of 40-50 ms. Addition of the non-N-methyl-D-aspartate (non-NMDA) selective antagonist 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX) to the slice surface near the recording electrode resulted in a rapid (within 30-45 s) suppression of the EPSP. Complete EPSP blockade was only slowly reversed by drug-free saline. Concentration-response relations (n = 14) showed 50% depression of EPSPs by surface concentrations of 1-10 microM CNQX. EPSP amplitude was resistant to the selective NMDA antagonist 2-amino-5-phosphonovalerate (AP 5) and, on average, was reduced less than 20% at 100 microM AP 5, an effect that was not statistically significant (n = 10; P greater than 0.05). In conclusion, this study offers the first direct evidence that EAAs mediate the primary events of afferent synaptic transmission in NTS. The experiments suggest that excitatory sensory afferent synaptic transmission to mNTS neurons is mediated by an EAA transmitter acting at non-NMDA receptors, but NMDA receptors may have a modulatory role.

2-Amino-5-phosphonovalerate↗
PubMed1990

Peptidergic modulation of mechanotransduction in rat arterial baroreceptors.

Regularly discharging baroreceptors in a rat in vitro aortic arch preparation were exposed to increasing concentrations of one of four vasoactive peptides: angiotensin II, arginine vasopressin, atrial natriuretic factor, or substance P. Slow ramps of pressure evoked discharge responses in single-fiber baroreceptors. Instantaneous discharge frequency was measured simultaneously with aortic diameter and pressure. During constriction induced by angiotensin II or arginine vasopressin, baroreceptor diameter threshold (Dth) decreased and pressure threshold (Pth) tended to increase; these effects were reduced or eliminated by nitroprusside. Atrial natriuretic factor and substance P by themselves were without effect on vessel diameter or on baroreceptor discharge. In preparations preconstricted with a moderate concentration of phenylephrine (10(-8) M), atrial natriuretic factor reduced the phenylephrine-induced constriction and increased Dth and decreased Pth. Substance P, even at high concentrations, was less effective than atrial natriuretic factor in reducing phenylephrine constriction and in altering baroreceptor discharge. Baroreceptor gain was unaffected by any of these peptides. Thus, changes in smooth muscle tone altered mechanotransduction by shifts in 1) the vessel pressure-diameter relation and 2) baroreceptor threshold requirements (Pth and Dth). Changes in the baroreceptor mechanical threshold (Dth) reduced the effects on Pth expected from changes in vessel wall mechanics. Pth reflects the net effects of vessel wall and Dth changes. Pth generally increased during constrictions and decreased during dilations. The changes in Dth and their selectivity (no changes in gain) during vasoactive peptide action closely resemble rapid resetting of baroreceptors. We propose that vascular smooth muscle lies in a parallel arrangement with aortic baroreceptors and that a common compensatory mechanism regulates Dth during sustained changes in vessel diameter. Activation of smooth muscle and reductions in transmural pressure would reduce loading of baroreceptors, and the proposed compensatory mechanism would tend to keep discharge constant by decreasing Dth. Our experiments, however, cannot distinguish between hypotheses for local micromechanical changes in coupling or for changes modulating excitability within the baroreceptor neuron itself as the basis for Dth adjustments.

Angiotensin II↗
PubMed1990

Dynamic and static conditioning pressures evoke equivalent rapid resetting in rat aortic baroreceptors.

A recent study suggested that exposure of carotid sinus baroreceptors to pulsatile pressures for a period of minutes can decrease the static threshold pressure at which they begin to discharge; that is, the exposure can sensitize baroreceptors. Another study found that the rapid resetting of carotid sinus baroreceptors to elevated conditioning pressures was reduced or eliminated by pulsatile conditioning. In the present study, we tested the responses of aortic baroreceptors in an in vitro preparation to a range of static and dynamic conditioning pressures lasting 15 minutes. Slow test ramps of increasing pressure were used to assess static discharge properties (threshold and gain). To be accepted for analysis (n = 12), each baroreceptor had to successfully complete static and dynamic test sequences for at least three different conditioning mean arterial pressure levels. We measured aortic diameter simultaneously with pressure and baroreceptor discharge. Generally, we found no significant difference between the static pressure threshold measured before and after dynamic conditioning. The static pressure threshold was linearly related to the mean level of the conditioning pressure, and no differences in the slopes of these relations (a measure of the ability of a baroreceptor to rapidly reset) were found between static and dynamic conditioning. After dynamic conditioning, discharge rates returned to near control levels in all cases within a few seconds of the return to static conditioning. Two baroreceptors exposed to the vasodilator nitroprusside throughout the experiment showed similar results. Diameter measurements indicated no role of vessel diameter changes during dynamic or static conditioning. In conclusion, we found no evidence of a long-lasting sensitization of aortic baroreceptors by dynamic pressure inputs.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1989

Arterial baroreceptor resetting: contributions of chronic and acute processes.

1. Pressure threshold (Pth) and suprathreshold pressure sensitivity (Sth) are important measures of the pressure-discharge characteristics of arterial baroreceptors. An in vitro preparation of the rat aortic arch-aortic nerve has been used to assess the influence of extracellular ion concentration, distensibility, smooth muscle activation and rapid resetting on single fibre baroreceptor discharge. 2. Changes in extracellular cations alter Pth and Sth in a reciprocal manner, suggesting that these two properties share common excitatory mechanisms probably at the level of membrane ion conductance channels. 3. During normal development and ageing in normotensive rats, Pth and blood pressure are fairly constant even during periods of greatly changing aortic distensibility. Sth increases progressively to maturity and then decreases somewhat with advanced age. 4. During hypertension, changes in distensibility in spontaneously hypertensive rats do not account for changes in Pth and Sth. 5. The capacity of arterial baroreceptors to rapidly reset during acute changes in the conditioning mean arterial pressure is not altered by chronic resetting, decreases in distensibility or by differences in the initial Pth or Sth of individual baroreceptors. 6. Within the maximal physiological or pathophysiological range, the prevailing or conditioning mean arterial pressure appears to be the most potent modulator of arterial baroreceptor discharge.

Aging↗
PubMed1989

Aberrant baroreceptor mechanotransduction in adult Dahl rats on low-salt diet.

Single fiber, regularly discharging baroreceptors (n = 118) from adult Dahl salt-sensitive (DS) and salt-resistant (DR) rats on a low-salt diet were studied using an in vitro aortic arch-aortic nerve preparation. Pressure thresholds (Pth) and suprathreshold pressure sensitivities (Sth) were determined from responses to slow ramps of pressure. Pressure-diameter relationships measured in each rat were used to transform Pth and Sth values to their mechanical equivalents in terms of aortic wall strain. DS and DR ages were not different (approximately 50 wk). Despite the low-salt diet, DS tail systolic blood pressures were significantly higher than DR by approximately 25 mmHg. Pth averaged 84 mmHg in DR and 97 mmHg in DS. Sth values were similar in DR and DS (average 1.44 and 1.39 spikes.s-1.mmHg-1 in DR and DS, respectively). Increased variance of baroreceptor properties of DS over DR was a prominent finding and necessitated use of nonparametric statistics. The cumulative distribution of Pth values of DS was significantly different from DR, but Sth values were similar. Thus baroreceptor pressure set points are altered in adult DS, but pressure sensitivity per se is not. The differences in pressure parameters were not eliminated by conversion to their mechanical equivalents. Correlation analysis found only weak relationships between Pth and blood pressure for DS and DR (r less than 0.40). Thus in contrast to previous studies in the spontaneously hypertensive rat model, baroreceptors in adult DS on low salt are characterized by elevated variability and a weaker than expected correlation to the prevailing blood pressure in the animal.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1989

Rapid baroreceptor resetting is unaltered by chronic hypertension in rats.

This study compares rapid baroreceptor resetting in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Single-fiber baroreceptor activity and aortic diameter were measured in in vitro preparations. Baroreceptor pressure threshold (Pth) and suprathreshold pressure sensitivity were measured during periods after various levels of conditioning mean arterial pressure (cMAP). The ability of a baroreceptor to reset was expressed as the resetting ratio (delta Pth/delta cMAP). Rapid resetting was successfully characterized in 30 baroreceptors (18 SHR and 12 WKY). SHR blood pressures were higher, and aortic distensibility was lower than in WKY. SHR baroreceptors showed signs of chronic resetting, i.e., elevated Pth (105.4 vs. 88.5 mmHg, SHR and WKY, respectively) and decreased suprathreshold sensitivity (0.92 vs. 1.42 spikes.s.-1.mmHg-1, SHR and WKY, respectively), but their resetting ratios were similar to WKY (0.260 and 0.237, SHR and WKY, respectively). Characterization of rapid resetting of more than one baroreceptor from single animals reveals that the resetting ratio can vary by greater than 50% within animals. During simultaneous discharge-diameter recordings, the strain threshold was better correlated to cMAP than Pth. We conclude that the ability of baroreceptors to rapidly reset is unaltered by chronic hypertension or chronic baroreceptor resetting, and we hypothesize that rapid resetting is probably a result of an intrinsic neural property rather than vessel mechanics.

Animals↗
PubMed1989

Interaction among unitary spike trains: implications for whole nerve measurements.

Interaction among action potential trains was examined in electroneurograms (ENGs) from filaments containing several fibers. In an in vitro preparation, increasing aortic pressure generated trains of action potentials (spikes) from regularly discharging aortic baroreceptors. Multifiber records were electronically sorted, and spikes from each separate baroreceptor were identified. "True" discharge rates, measured as the instantaneous frequency of the sorted records, were compared with the results of three quantitation approaches commonly used for multifiber or whole nerve activity in mass ENGs: "spike" counts per unit time, ENG voltage integration, and normalizations of counts or integration. Even in ENGs containing only two active baroreceptors, numerous interactions of the two spike trains occurred. Of 33 paired recordings (66 baroreceptors), 77.3% of the individual baroreceptors had spike trains that could not be clearly discriminated because of interactions with signals from other baroreceptors. Virtually all baroreceptors (96.3%) in nine three-fiber ENGs (27 baroreceptors) showed evidence of missed spikes. Corrected or true spike rates were always greater than activity rates measured by simple counting. Similarity of discharge frequencies in the different baroreceptors was the most important determinant of the rate of voltage signal interaction. Simple count or integration methods underestimated slopes of pressure-response curves and peak activity values by 20-40% compared with sorted instantaneous frequency. Not all coincidence of action potentials in the ENG resulted in simple additions of peak voltages. We conclude that simple counting and integrative techniques substantially underestimate multifiber nerve activity and such quantitation techniques should be used cautiously, particularly in experimental comparisons across groups of animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1989

High-salt diet elevates baroreceptor pressure thresholds in normal and Dahl rats.

Dahl Salt Sensitive (DS) rats rapidly develop high blood pressure when exposed to a high-salt diet. Recent studies suggest that DS rats have poorly functioning baroreceptor afferents and baroreflexes even when salt intake is restricted. This study examines baroreceptor pressure- and mechano-transduction in DS, Dahl Resistant (DR), and Sprague-Dawley (SD) rats during low- and high-salt conditions. Single unit, regularly discharging baroreceptors were studied using an in vitro aortic arch-aortic nerve preparation. Pressure thresholds and suprathreshold pressure sensitivities were determined from responses to slow ramps of pressure. Pressure-diameter relations measured in each rat were used to transform pressure threshold and pressure sensitivity values to their mechanical equivalents in terms of aortic wall strain. A total of 407 unit baroreceptors were studied from 49 rats. Tail systolic blood pressures were significantly higher only in DS during high salt. Pressure threshold was similar for all groups on low salt. Exposure to a high-salt diet increased the mean pressure threshold for all three groups. Pressure threshold for high-salt diet was highest in DS and lowest in DR. Pressure sensitivities were lowest in DS and highest in DR on low salt. High salt had no significant effect on pressure sensitivity. The differences in threshold apparent when expressed in terms of pressure were eliminated by conversion to their mechanical equivalents (strain threshold and strain sensitivity). The results suggest that baroreceptors in the two Dahl rat strains represent two extremes from normal baroreceptor function. DS tend to be less pressure responsive than normal (SD), and DR tend to be somewhat more responsive to pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1987

Ionic sensitivity of baroreceptors.

Baroreceptors respond to distortion of their receptor regions by producing action potentials and, thus, provide information to the central nervous system for cardiovascular control. The mechanisms converting mechanical events to electrical signals are unknown. Since it has not been possible to record a receptor potential in the mechanosensitive terminals, studies rely on interpretation of axonal discharge of baroreceptor endings. In the present study, the ionic sensitivity of in vitro preparations of both low- and high-pressure receptors are compared in studies in which the ionic composition of the extracellular fluid is controlled. The results taken together with previous work suggest uniformity of response to calcium, sodium, and potassium across a variety of cardiovascular receptor types supporting common mechanoelectrical transduction mechanisms. Decreased extracellular sodium produced increased threshold and decreased slopes of pressure-discharge curves for both aortic arch baroreceptors and for low-pressure baroreceptors in the atrium. Results are consistent with data for other mechanoreceptors where it is believed that distortion activates a relatively poorly selective cation-conducting channel through the membrane. As with arterial baroreceptors, increases in external calcium levels caused a decrease in the excitability of atrial baroreceptors. Substitution of half the external calcium with the inorganic calcium channel blocker cobalt failed to alter baroreceptor function. Bay K 8644, a calcium channel agonist of the dihydropyridine class of calcium channel blockers, tended to inhibit baroreceptor discharge with effects consistent with smooth muscle activation within the vessel wall. Several hypotheses of potential underlying mechanisms are discussed. These new experiments are consistent with the results achieved with alterations of ionic calcium and suggest that calcium entry does not play a detectable role in baroreceptor transduction.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1986

Do calcium antagonists act directly on calcium channels to alter baroreceptor function?

This study examined the effects of antagonists known to act on voltage-dependent calcium channels (chiefly nitrendipine, diltiazem and verapamil) on arterial baroreceptor function. Single fiber discharge of aortic arch baroreceptor preparations of the rat was not altered at concentrations ranging from 10(-11) to 10(-6) M. Increasing pressure in an isolated perfused carotid sinus in the cat produced a reflex arterial pressure response which was not altered significantly when the carotid perfusate contained an antagonist concentration of 10(-7) to 10(-6) M. A higher concentration (10(-5) M) of all three antagonists decreased baroreceptor discharge and depressed the reflex response. In addition, nimodipine and nifedipine had uniformly similar dose-related effects. It is likely that the effects found at the elevated concentrations are nonspecific and probably are independent of voltage-dependent calcium channels. No differences between the dihydropyridine blockers and verapamil were found even at very high doses. Our results suggest that within the range of doses used clinically these antagonists do not directly affect baroreceptor function. In addition, the present results reinforce the notion that voltage-dependent calcium channels are not importantly involved in baroreceptor transduction as suggested by earlier studies of the effects of changing external calcium concentration.

Animals↗
PubMed1984

Short- and long-term determinants of baroreceptor function in aged normotensive and spontaneously hypertensive rats.

In a variety of animal models, baroreceptor resetting during chronic hypertension has been correlated to vessel wall hypertrophy and decreased distensibility. In one possible mechanism of chronic resetting, termed the splinting hypothesis here, it has been suggested that a stiffer vessel wall might increase the minimum pressure required for activation of these mechanoreceptors (pressure threshold) and decrease suprathreshold pressure sensitivity. Lower vessel distensibility would alter baroreceptor function by preventing equivalent pressures from producing equivalent vessel distensions and, thus, receptor distortions. Recent studies have also suggested that the pressure threshold is strongly influenced by the most recent (minutes) history of blood pressure exposure during a process termed rapid resetting. Hypertension and advanced aging are associated with distensibility changes. The present study examines pressure and equivalent mechanical response characteristics of aortic baroreceptors from aged normotensive Wistar-Kyoto and spontaneously hypertensive rats. An in vitro aortic arch-aortic nerve preparation was used to assess the discharge properties from a number of baroreceptors and the pressure-diameter relationship of each aorta. Both control and rapid resetting protocols were used to study the baroreceptor characteristics. Aged Wistar-Kyoto rats were normotensive and averaged 115 weeks of age. Aged spontaneously hypertensive rats had systolic tail pressures of 187 mm Hg and averaged 76 weeks of age. Although aortic distensibility of aged WKYs was much lower than previously found in younger animals, the pressure threshold was unchanged. Aged spontaneously hypertensive rat receptors were chronically reset in proportion to their blood pressure. Decreased distensibility did not alter the rapid resetting process. It is concluded that baroreceptor pressure sensitivity is more closely related to aortic distensibility under several conditions altering vessel stiffness, whereas, the pressure threshold may be regulated additionally by mechanisms independent of distensibility. The results are inconsistent with the splinting hypothesis.

Aging↗
PubMed1983

Resetting of aortic baroreceptors with non-myelinated afferent fibers in spontaneously hypertensive rats.

The phenomenon of resetting and the possible mechanisms responsible for it were investigated in aortic baroreceptors having unmyelinated axons. Recordings were obtained from 31 aortic baroreceptor C-fibers in 20 normotensive Wistar Kyoto rats (WKY) and 37 baroreceptor C-fibers in 11 spontaneously hypertensive rats (SHR). The recordings were obtained from the left aortic nerve of an in vitro aortic nerve-aortic arch preparation. The thresholds for activation of baroreceptor C-fibers were not different between SHR's and WKY's at 16 weeks of age (139 +/- 7 and 133 +/- 5 mmHg, respectively). However, the thresholds for activation in SHR at 36 weeks of age were considerably higher (163 +/- 4 mmHg) indicating resetting of the receptors in the older rats. The pressure-discharge curves were not different between SHR's and WKY's at 16 weeks of age and WKY's at 35 weeks of age, but were shifted to the right for SHR's at 36 weeks of age. The receptors showed greater responses to pulsatile pressures than to steady state pressures at the same mean level of pressure. We found that aortic C-fibers were not reset during the early established phase of hypertension in SHR's because of enhanced receptor strain sensitivity. This is likely to be of importance for tonic vasomotor control at this time. In later stages of hypertension and despite enhanced strain sensitivity the endings were reset to higher pressures probably due to an increased collagen content in the aortic wall.

Animals↗
PubMed1983

Rapid resetting of aortic baroreceptors in vitro.

Pressure-response characteristics of arterial baroreceptors (BR) were shown recently to be reset following a 15- to 20-min change in mean arterial pressure (MAP); the curves shifted in the direction of the MAP change. To characterize this rapid BR resetting process more precisely than in vitro studies allow, we utilized an in vitro aortic arch-aortic nerve preparation from Wistar-Kyoto rats. Pressure ramps were used to determine the discharge response curves of single BRs following exposure to precisely controlled conditioning pressures. Rapid resetting occurred in all BRs and followed an exponential time course with a 3- to 5-min time constant. The reset curves were stable for 1 h and were completely reversible. The curves were shifted along the pressure axis in a parallel manner, i.e., pressure threshold (Pth) changed but slope and mean asymptotic discharge were unaltered. In experiments lasting as long as 7 h in which more than two MAP steps were possible, in vitro rapid resetting was a very consistent and reproducible process. Quantitatively, the extent of resetting (delta Pth/delta MAP) averaged 0.33 over an MAP range of 40-160 mmHg. In vitro resetting therefore appears very similar to that observed in vivo, suggesting that the conditioning pressure is the primary, perhaps the sole, determinant of resetting. Resetting occurred at subthreshold MAPs, demonstrating action potentials are not a prerequisite. Efferent neural or hormonal influences are also not required.

Acclimatization↗