Biomedical subjects

B N Van Vliet

Publications and source records attributed to B N Van Vliet.

At least 19 recordsLinked to original sources

PubMed2001

Loss of nocturnal dipping of blood pressure and heart rate in obesity-induced hypertension in rabbits.

We have investigated in rabbits whether overfeeding and weight gain, which lead to hypertension, are associated with changes in circadian rhythm of blood pressure (BP) and heart rate, and whether the sympathetic nervous system is involved in these changes. In adult male rabbits, mean arterial pressure (MAP) and heart rate (HR) were monitored by telemetry 22 h a day. Daily MAP and HR records were divided into four equal intervals and used to calculate day-night differences. After a 1-week control period, animals were switched to a high-fat (HFD) ad libitum diet for 8 weeks. HFD increased whole day MAP and HR, and rapidly abolished the normal diurnal rhythm of MAP and HR. Since HFD abolished the nocturnal dip in MAP, but had little effect on daytime values, the loss of dipping appears to account for most of the hypertension in this model of obesity. In a separate set of rabbits, alpha- and beta-adrenergic blockade (terazosin + propranolol) prevented HFD-induced hypertension and attenuated the increase in HR by more than half. Adrenergic blockade alone abolished the diurnal rhythm of MAP, chiefly by preventing daytime elevation of MAP. The addition of HFD ad libitum did not further modify daily MAP or its circadian pattern. The diurnal rhythm of HR was relatively unaffected by alpha + beta blockade alone, but was abolished after switching to HFD. In conclusion, rabbits fed an HFD ad libitum develop hypertension and tachycardia associated with a loss of the normal diurnal rhythm of MAP and HR. The hypertension appears to be sympathetically mediated.

Adrenergic alpha-Antagonists↗

PubMed2000

Role of the sympathetic nervous system during the development of obesity-induced hypertension in rabbits.

We have previously reported that weight gain induced by high-fat diet (HFD) leads to an increase in mean arterial pressure (MAP, +14%) and heart rate (HR, +31%) in the adult rabbit. In the present study, we tested the hypothesis that an increased activity of the sympathetic nervous system may contribute to the development of obesity-induced hypertension. A combination of alpha- and beta-adrenergic blockers (terazosin + propranolol) was chronically administered to rabbits housed in metabolic cages for continuous monitoring of arterial pressure by telemetry, 24 h a day. After 2 weeks of adrenergic blockade under control diet, animals were switched to HFD for the next 6 weeks. HFD induced a progressive increase in body weight, but no increase in mean arterial pressure (+0.2+/-2.5%) and a slight increase in heart rate (+14+/-3%). Time-control animals fed normal diet showed no changes in MAP or HR with long-term alpha- and beta-adrenergic blockade. Our results indicate that the activation of the sympathetic nervous system may play an important role in the pathogenesis of obesity-induced hypertension.

Adrenergic alpha-Antagonists↗

PubMed1999

Contribution of baroreceptors and chemoreceptors to ventricular hypertrophy produced by sino-aortic denervation in rats.

1. To test whether sino-aortic denervation (SAD)-induced right ventricular hypertrophy (RVH) is a consequence of baroreceptor or chemoreceptor denervation, we compared the effects of aortic denervation (AD), carotid denervation (CD), SAD and a SAD procedure modified to spare the carotid chemoreceptors (mSAD), 6 weeks after denervation surgery in rats. A sham surgery group served as the control. 2. The blood pressure (BP) level was unaffected by AD, CD or SAD, but increased (9 %) following mSAD. The mean heart rate level was not affected. Short-term BP variability was elevated following AD (81 %), SAD (144 %) and mSAD (146 %), but not after CD. Baroreflex heart rate responses to phenylephrine were attenuated in all denervation groups. 3. Significant RVH occurred only following CD and SAD. These procedures also produced high mortality (CD and SAD) and significant increases in right ventricular pressures and haematocrit (CD). 4. Significant left ventricular hypertrophy occurred following CD, SAD and mSAD. Normalized left ventricular weight was significantly correlated with indices of BP variability. 5. These results suggest that SAD-induced RVH is a consequence of chemoreceptor, not baroreceptor, denervation. Our results also demonstrate that a mSAD procedure designed to spare the carotid chemoreceptors produced profound baroreflex dysfunction and significant left, but not right, ventricular hypertrophy.

Adrenergic alpha-Agonists↗

PubMed1996

Cardiac hypertrophy and telemetered blood pressure 6 wk after baroreceptor denervation in normotensive rats.

We investigated cardiac morphometry 6 wk after sinoaortic baroreceptor denervation (SAD) in Long-Evans rats. SAD (n = 19) was associated with an 11% increase in the weight of the left ventricle (LV) plus septum (P < 0.001) and a 39% increase in that of the right ventricular (RV) free wall (P < 0.001), relative to sham-operated rats (n = 18). RV wall thickness was significantly increased in SAD animals, but there was no difference in the LV wall thickness and volumes of the RV and LV between groups. Constrictor responses to methoxamine and dilation responses to acetylcholine were assessed in an in vitro perfused mesenteric circulation preparation, but neither response was affected by SAD. Baroreceptor denervation was associated with marked and significant increases in the variability (2.8-fold) and daily peak (39 mmHg) levels of telemetered mean arterial pressure (MAP) and small (5%) but significant increases in the daily mean MAP level. Our results are consistent with an effect of increased MAP variability on ventricular weight but cannot rule out possible contributions from other mechanisms.

Animals↗

PubMed1995

Obesity and hypertension: roles of hyperinsulinemia, sympathetic nervous system and intrarenal mechanisms.

Hypertension is a well-recognized complication of obesity. However, the mechanisms for the development of obesity hypertension are not known. One mechanism proposed is that the hyperinsulinemia present in obese hypertensive patients causes hypertension via sodium retaining and/or sympathetic nervous system stimulatory effects. However, numerous studies in dogs have revealed no evidence for such chronic pressor actions of hyperinsulinemia. This is in close agreement with studies in human insulinoma patients that show marked hyperinsulinemia and normal blood pressure. The appropriateness of the dog as an experimental model is strengthened by reports from our laboratory and others that inducing obesity in dogs reproduces many of the characteristics of obesity in humans, including insulin resistance, hyperinsulinemia, sodium retention, hypertriglyceridemia and hypertension. Recent studies in obese dogs have indicated that significant increases in renal medullary cellularity and intercellular matrix deposition could contribute to the sodium retention and hypertension. Additional evidence suggests that sympathetic nervous system stimulation also may contribute to the elevated blood pressure. However, the mechanisms through which obesity induces these changes and the temporal relationship between these factors and the development of the hypertension remains to be determined.

Animals↗

PubMed1995

Effect of denervation of the rat superior mesenteric arterial bed on the distribution of resistance among the first four orders of branching.

The rat superior mesenteric artery with its first four orders of branching has been examined as an isolated perfused preparation. Lumen diameter and proportional resistance at each level have been determined and compared under conditions of constant pressure following methoxamine-induced constriction and acetylcholine-induced relaxation in intact and denervated preparations. A comparison was also made between intact preparations under conditions of constant pressure and constant flow. Lumen diameter and segment length were measured by analysis of video-taped images. The distribution of resistance among the first four orders of branching was estimated from the measured values using the Poiseuille formula. Intact first and fourth order branches had a proportionately low resistance, with the remaining resistance being fairly evenly distributed between the second and third order branches. No change in the pattern occurred as a result of either methoxamine or acetylcholine treatment. The pattern of distribution of resistance changed following denervation, so that proportional resistance was high in the first order branches and fell off from the second to fourth order branches. With methoxamine, the first order branches of denervates had a significantly higher resistance than in intact tissues, with the distribution of resistance in the second to fourth order branches following the basal resistance pattern. Reduction in the proportion of resistance with acetylcholine was similar in both intact and denervated preparations. Distribution of resistance did not differ between constant flow and constant pressure intact preparations.

Acetylcholine↗

PubMed1995

Reduced parasympathetic control of heart rate in obese dogs.

We investigated why resting heart rate is elevated in dogs fed a high saturated fat diet for 12.7 +/- 1.8 wk. Obese dogs exhibited elevated body weight (59%), blood pressure (14%), and heart rate (25%). Differences in resting heart rate (control, 58 +/- 5 beats/min; obese, 83 +/- 7 beats/min) were abolished after hexamethonium, indicating an autonomic mechanism. Hexamethonium also reduced blood pressure in obese (20 +/- 4 mmHg) but not control (9 +/- 6 mmHg) animals. Propranolol did not affect heart rate in either group, excluding a beta-adrenergic mechanism. Subsequent administration of atropine increased heart rate more in control than in obese dogs (110 +/- 9 vs. 57 +/- 11 beats/min). The sensitivity of the cardiac limb of the baroreflex (Oxford method) was reduced by 46% in the obese group, confirming impairment of the parasympathetic control of heart rate. The standard deviation of blood pressure measurements was normal when expressed as a percentage of the mean arterial blood pressure (control, 11.2 +/- 0.4%; obese, 11.2 +/- 0.5%). Our results indicate that the development of obesity in dogs fed a high saturated fat diet is accompanied by an attenuated resting and reflex parasympathetic control of heart rate.

Animals↗

PubMed1995

Advantages of continuous measurement of cardiac output 24 h a day.

To test the hypothesis that continuous measurement of cardiac output 24 h a day would provide a better day-by-day reproducibility of the daily average cardiac output than acute measurements, we developed a computer-assisted method to monitor cardiac output continuously using an electromagnetic flow transducer. Because the diastolic aortic flow, which is used as a zero-flow reference, can drift significantly with electromagnetic flow probes, automatic tracking of the diastolic flow baseline was considered essential for long-term measurements. To accomplish this, the analog pulsatile flow signal was digitally converted and processed by an IBM PC to correct for signal drift on a beat-per-beat basis. Using this computerized system in 19 chronically instrumented dogs, we compared the values of cardiac output during 5 consecutive control days, measured either for 20 h each day (allowed 4 h for special care) or for 30 min in the morning when the trained dogs were required to lie quietly in their cages. The results show that the coefficient of variation of the five daily averages in cardiac output for each individual dog was three times smaller when cardiac output was measured 20 h each day (2.9 +/- 0.3 vs. 9.7 +/- 1.0%). Whole-day coefficients of variation were also smaller for mean arterial pressure, heart rate, stroke volume, and total peripheral resistance. Because of this greater day-by-day reproducibility, continuous monitoring of cardiac output is likely to be more sensitive to small changes in cardiac output induced by experimental protocols.

Animals↗

PubMed1994

Hypertension induced by nitric oxide synthesis inhibition is renal nerve dependent.

Recent studies have indicated that chronic administration of N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthesis, produces marked hypertension. Although the mechanism of this form of hypertension is not well understood, several studies have demonstrated that sympathetic nerve activity is at least acutely elevated after L-NAME administration. To evaluate the potential role of the renal sympathetic nerves in L-NAME-induced hypertension, we compared the blood pressure response to L-NAME in four groups of Sprague-Dawley rats (n = 8 each): (1) sham-operated vehicle-treated, (2) sham-operated L-NAME-treated, (3) denervated vehicle-treated, and (4) denervated L-NAME-treated. After renal denervation or sham surgery, L-NAME was added to the drinking water (70 mg/100 mL) for 4 weeks, and arterial pressure was measured weekly by the tail-cuff method. L-NAME treatment caused a progressive increase in arterial pressure in sham-operated rats, rising to 154 +/- 6 mm Hg by week 4 of treatment compared with 115 +/- 2 mm Hg in the vehicle-treated sham-operated group (P < .005). In contrast, the development of hypertension was significantly delayed and attenuated in renal-denervated rats treated with L-NAME. The results of our study suggest that L-NAME-induced hypertension may be partly mediated by or is at least dependent on the integrity of the renal nerves.

Animals↗

PubMed1992

Migraine with aura: a vicious cycle perpetuated by potassium-induced vasoconstriction.

Two hypotheses have dominated attempts to understand the etiology of migraine with aura or classic migraine; the vascular spasm model proposed by Wolff and colleagues, and the spreading cortical depression hypothesis. Neither can provide a fully satisfactory explanation for the syndrome, however. We propose that classic migraine is both spreading cortical depression and localized ischemia linked in a vicious cycle by potassium induced vasoconstriction. The cycle can be initiated by any event which raises the local cortical ECF potassium concentration to approximately 20 mM. Such an event could be a localized burst of activity of a group of cells, localized metabolic impairment, or a transient reduction in blood flow to a region of the cortex. Once this level of potassium concentration is reached, it may result in localized depolarization of neurons, releasing more potassium into the ECF. Glial siphoning can distribute the potassium preferentially toward the blood vessels in the area, leading to an elevation in potassium concentration in the ECF surrounding the vascular smooth muscle of the arterioles. Above approximately 15 mM, vascular smooth muscle increases its tension in response to elevations in potassium. Therefore, as cortical ECF potassium concentration rises above 15 to 20 mM, localized vasoconstriction occurs, thereby reducing both the supply of oxygen for aerobic metabolism and the removal of potassium in the blood. Under these conditions, the effectiveness of the mechanisms which control potassium concentration is impaired and unable to prevent additional elevations in potassium. As the concentration continues to rise, vasoconstriction becomes more intense, perpetuating the cycle that results in localized depression of cortical neuronal activity and ischemia. The condition is propagated to adjacent regions of the cortex by diffusion and glial-mediated spread of potassium. In many respects, the hypothesis unites the vascular spasm and spreading depression models. If verified, it may provide insight into the causes of classic migraine as well as give direction toward development of effective therapies.

Humans↗

PubMed1992

Antagonistic interaction of laryngeal and central chemoreceptor respiratory reflexes.

Stimulation of laryngeal afferent fibers evokes a profound reflex inhibition of central respiratory drive. The interaction of this airway reflex with chemoreceptive ventilatory control mechanisms is poorly understood. The present study was undertaken to determine whether there is significant interaction between the effects of central chemoreceptor and laryngeal afferent stimulation on central inspiratory activity and, if so, to also determine the nature of the interaction. The effect of electrical stimulation of the superior laryngeal nerve (SLN) on the timing and intensity of central inspiratory activity was determined from the rectified and filtered phrenic neurogram in 10 dogs. Each dogs was decerebrated, artificially ventilated, vagotomized, and had the carotid bodies denervated. In each case, stimulation of the right SLN at 3 and 10 Hz caused a frequency-dependent slowing or arrest of central inspiratory activity. Increases in arterial PCO2 (PaCO2) attenuated the absolute level of inhibition of central inspiratory activity recorded during both SLN stimulation and control periods. Tp clarify the nature of the interaction between chemoreceptor and laryngeal afferent stimulation, the relationship between PaCO2 and central inspiratory activity was investigated during stimulation of the SLN at 0, 3, and 10 Hz. Control central inspiratory activity increased as a sigmoidal function of PaCO2. This sigmoidal relationship was greatly depressed during SLN stimulation but did not appear to be shifted along the PaCO2 axis. The results of this study therefore suggest that the interaction between central chemoreceptor and laryngeal afferent stimulation is multiplicative: the inhibition of the central inspiratory activity is mediated by an attenuation and not a resetting of central chemoreflexes.

Afferent Pathways↗

PubMed1991

Time course of renal responses to greater splanchnic nerve stimulation.

The objective of the present study was to describe the time courses of renal responses during renal sympathetic stimulation and to determine whether the kidney can provide a sustained response to sympathetic stimulation for 3 h. In four pentobarbital sodium-anesthetized dogs, stimulation (3.3 Hz) of a greater splanchnic nerve (GSN) on one side caused reductions in renal blood flow (RBF) and sodium excretion (UNaV) of both stimulated and contralateral-denervated kidneys, plus an increase in plasma renin activity (PRA). During continued stimulation, RBF partially recovered, but UNaV fell to less than 5% of control and PRA rose and remained at least eight times above control. In nine dogs, a single GSN was stimulated after ipsilateral adrenal medullectomy and ligation of the splanchnic circulation. The acute response to GSN stimulation was now confined to the ipsilateral kidney. Ipsilateral RBF fell by 32 +/- 10% but returned to 85 +/- 5% of control values by the end of the stimulation period. Contralateral RBF fell slowly by approximately 10%. Ipsilateral and contralateral UNaV fell to 34 +/- 10 and 43 +/- 11% of control values, respectively. PRA increased rapidly at the onset of GSN stimulation and remained at least 2.8 times control levels. After stimulation, RBF, UNaV, and PRA returned toward control levels. These results confirm the findings of others that the response of the renal vasculature to sympathetic stimulation is mainly transient. However, they additionally demonstrate a strong and sustained decrease in UNaV lasting for the total 3-h period of sympathetic stimulation.

Adrenal Medulla↗

PubMed1989

Cardiovascular responses to denervation of pulmocutaneous baroreceptors in toads.

Toad pulmocutaneous arterial baroreceptors are connected to afferent fibers carried in the recurrent laryngeal nerves (rLNs). Bilateral rLN denervation in conscious toads (Bufo marinus) caused 34 and 78% increases in heart rate (Fh) and systemic arterial blood pressure (Pa) within 10-15 min, respectively. The variance of Pa was significantly increased 2 days after denervation, but Pa and Fh were not. In additional chronic experiments, 5 of 17 baroreceptor-denervated toads died within the 2-wk recovery period. No deaths occurred in sham-operated toads. The mean Pa, Fh, and cardiac interval (Ic), the mean variance of Pa, Fh, and Ic, and Pa and Fh responses to stress, plasma composition, and the dry-to-wet weight ratio of skeletal muscle and lung were not statistically different in denervated and sham-operated toads. However, the sensitivity of Ic to changes in Pa, exposed by intra-arterial injections of phenylephrine and nitroprusside, was attenuated in denervated toads. Postmortem examination revealed occasional pulmonary lesions, the incidence of which appeared correlated with causes of pulmonary hypertension: baroreceptor denervation and phenylephrine injections. We conclude that pulmocutaneous arterial baroreflex is tonically active but is not essential for the long-term maintenance of Pa in conscious undisturbed toads.

Animals↗

PubMed1987

Measurement of signal period on a personal microcomputer and its application to the analysis of cardiac interval and blood pressure.

Personal microcomputers interfaced with analog-digital converters are capable of analyzing almost any biological signal, yet are limited in their ability to directly measure a signal's period/frequency. We describe a short program which measures the interval between periodic events up to 3.5 Hz. In addition, an expanded program which calculates the frequency distribution, distribution statistics, and cross regressions of cardiac interval and blood pressure is described.

Analog-Digital Conversion↗

PubMed1987

Hypoxemic threshold for lung ventilation in the toad.

The relationship between the activity of the buccal force pump, expressed as the time integral of positive buccal pressure, and PaO2 was investigated in conscious toads, Bufo marinus, unidirectionally ventilated at a high flow rate (240-260 ml/min). The high ventilatory flow rate meant that PaO2 was largely independent of the animal's ventilatory activity so that the relationship between pulmonary ventilation and PaO2 was effectively open-loop. The hypoxemic threshold (PaO2) for lung ventilation was 54.2 mm Hg in hypocapnia (PaCO2 = 4.7 +/- 0.3 mm Hg), 82.6 mm Hg in normocapnia (PaCO2 = 11.6 +/- 0.2 mm Hg), and 137.9 mm Hg in hypercapnia (PaCO2 = 20.1 +/- 0.1 mm Hg). Unidirectional ventilation with 20% O2 in N2, a condition in which the toads were normoxic but hypocapnic, stopped pulmonary ventilation cycles. Taken with existing evidence that hyperoxia stops pulmonary ventilation even under conditions in which PaCO2 is elevated this suggests that hypoxic and hypercapnic stimuli summate to drive lung ventilation in the toad. Bilateral denervation of the carotid labyrinths decreased pulmonary ventilation in absolute terms, but did not reduce the proportionate increase in pulmonary ventilation in response to normocapnic hypoxia, suggesting that chemoreceptors within the carotid labyrinth may contribute to, but are not solely responsible for, the hypoxemic ventilatory drive.

Animals↗

PubMed1987

Responses to circulatory pressures, and conduction velocity, of pulmocutaneous baroreceptors in Bufo marinus.

1. Baroreceptor activity was recorded within the recurrent laryngeal branch of the toad vagus in forty-four preparations. The receptive fields of the receptors were located in the pulmocutaneous artery (p.c.a.), generally within 5 mm of its separation from the truncus. However, the most easily recorded afferents in this nerve were mechanoreceptors which responded to punctate stimulation of the lip of the glottis. 2. The conduction velocities of p.c.a. baroreceptor and mechanoreceptive glottal afferents recorded in the recurrent laryngeal nerve ranged from 0.3-0.7 (0.5 +/- 0.1) m s-1 and 2.2-14.0 (6.8 +/- 0.8) m s-1 respectively, which suggests that baroreceptor afferent fibres are non-myelinated and that glottal afferent fibres are myelinated. 3. The p.c.a. baroreceptor discharge was largely confined to a period of systole in which systemic and p.c.a. arterial pressure profiles were identical. The maximum discharge frequency, number of spikes per cycle, and the duration of discharge increased, and the discharge latency decreased, as p.c.a. pressures were elevated. The latency of the discharge was pronounced at low p.c.a. pressures, and could be partially accounted for by the conduction time of the baroreceptor afferents to the electrodes (up to 100 ms). 4. Carotid and aortic arterial baroreceptor and pharyngeal afferents were recorded in two pharyngeal branches of the vagus nerve which were closely associated with the carotid and aortic arterial arches. 5. It is suggested that baroreceptor populations with their receptive fields in the third- (carotid) and sixth- (p.c.a. or pulmonary) arch arteries should be considered homologous in anurans and mammals, but that those of the fourth- (aorta) arch artery should not, since the vagal branches in which their afferents are carried do not appear to be equivalent in anurans and mammals.

Action Potentials↗

PubMed1987

Response characteristics of pulmocutaneous arterial baroreceptors in the toad, Bufo marinus.

1. Response characteristics of baroreceptors with receptive fields in the pulmocutaneous artery (p.c.a.) were determined in pithed toads by applying pressure steps, ramps, sine waves, and volume infusions into the vascularly isolated and perfused p.c.a. 2. The baroreceptors exhibited phasic and tonic discharge thresholds (30.3 +/- 2.3 and 36.2 +/- 2.8 mmHg respectively) which were above mean arterial pressure values reported for conscious undisturbed toads. They are comparable, in this respect, to non-myelinated mammalian arterial baroreceptors. 3. The maximum-phasic and minimum-adapted discharge frequencies of the p.c.a. baroreceptors were low (30 and 2-3 spikes s-1, respectively), but resembled those reported for mammalian non-myelinated baroreceptors when an adjustment was made for the difference in the temperature of mammalian and amphibian preparations. 4. The sensitivity of the baroreceptor discharge frequency to pressure (delta F/delta P) was estimated from pressure-step and pressure-ramp stimuli. Both estimates were greater than those reported for mammalian systemic arterial baroreceptors after the values were normalized to the maximum discharge frequency of the receptors. delta F/delta P and saturation discharge frequency values estimated from ramp stimuli increased with the dP/dt of pressure ramps. 5. The diameter of the p.c.a. was measured by sonomicrometry in toads anaesthetized with urethane. The diameter pulsation was 7.7 +/- 0.3% of the mean diameter (3.5 +/- 0.1 mm) at a mean pulse pressure of 22 +/- 1 mmHg, and Peterson's pressure-strain modulus was calculated to be 4.0 X 10(5) +/- 0.3 X 10(5) dyn cm-2, which suggests that the p.c.a. is highly compliant, and in this respect is comparable to the pulmonary artery, but not to systemic arteries, in mammals. Baroreceptor discharge began near the point of peak dynamic compliance (dV/dP) and continued as dV/dP decreased. Increasing the rate of infusion reduced the peak dV/dP, but increased the baroreceptor discharge frequency. 6. The response to sinusoidal oscillating pressure stimuli was distorted by rectification. Increasing the frequency of sinusoidal stimulation over the range 0.05-1.0 cycles s-1 reduced the number of spikes per cycle, but increased the mean discharge frequency.

Action Potentials↗

PubMed1987

Ventilatory effects of stimulation of phrenic afferents.

The diaphragm, a ventilatory muscle, has abundant sensory innervation. The effects of phrenic afferent activation on ventilation have been varied. In this study the proximal end of the phrenic nerve was electrically stimulated, and the effects on ventilation were measured in supine dogs anesthetized with either alpha-chloralose or pentobarbital sodium. We found a maximum increase in ventilation of 45 +/- 4% in the alpha-chloralose group and an increase in mean arterial blood pressure of 18 +/- 4%. This response was obtained at high stimulus intensities (60 times twitch threshold). Stimulation of the proximal end of the gastrocnemius nerve produced a similar ventilatory response (61 +/- 10%) but at lower stimulus intensities. During pentobarbital sodium anesthesia both the hyperventilation and the pressor response were produced; however, ventilation was increased by an increase in respiratory frequency. The reflex was abolished by sectioning of the cervical dorsal roots (C4-C7). Proximal cold blockade of the nerve abolished the response at a perineural temperature of 1.35 +/- 0.64 degrees C. The main effect of activation of phrenic afferents was an increase in ventilation and blood pressure that was mediated by unmyelinated fibers and possibly thin myelinated fibers. This response is similar to skeletal muscle afferent activation and may play a role in ventilatory drive during such conditions as exercise and respiratory muscle fatigue.

Afferent Pathways↗