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Biomedical subjects

F R Calaresu

Publications and source records attributed to F R Calaresu.

At least 37 records · Page 2Linked to original sources
PubMed1991

Monosynaptic connection from caudal to rostral ventrolateral medulla in the baroreceptor reflex pathway.

Experiments were done to test the hypothesis that caudal ventrolateral medulla (CVLM) neurons excited by activation of arterial baroreceptors and by stimulation of depressor sites in the nucleus tractus solitarii (NTS) project monosynaptically to the rostral ventrolateral medulla (RVLM). In urethan anaesthetized and artificially ventilated rats we recorded extracellular activity from 46 spontaneously firing units in the CVLM. Twenty of these units were excited by baroreceptor activation (1-3 micrograms phenylephrine i.v.) and of these 6 were excited (mean latency of 9.8 +/- 2.3 ms) by single pulses (0.1 ms, 30 +/- 8.3 microA) delivered once per second to a depressor site in the ipsilateral NTS. These 6 units were also antidromically activated with a latency of 4.1 +/- 0.12 ms by stimulation of a pressor region in the ipsilateral RVLM. These results provide evidence for the existence of an excitatory projection from the NTS to the CVLM which, in turn, projects monosynaptically to sympathoexcitatory neurons in the RVLM.

Action Potentials↗
PubMed1991

Cardiovascular responses to combined microinjection of substance P and acetylcholine in the intermediolateral nucleus of the rat.

As microinjection of either substance P (SP) or acetylcholine (ACh) into the right intermediolateral cell nucleus (IML) at the T2 level elicits increases in heart rate (HR) in the anesthetized rat, we investigated the possibility of a synergistic effect on HR and arterial pressure (AP) of ACh and SP microinjected in this nucleus. Moreover, we studied the effect on HR and AP of microinjection of either ACh or SP into the IML combined with activation of cardiovascular neurons in the ipsilateral rostral ventrolateral medulla (RVLM) by microinjection of glutamate (Glu). Male Wistar rats (n = 16) were anesthetized with urethane (1.4 g/kg i.p.), artificially ventilated, and the dorsal medulla and spinal cord (T1-T3) were exposed. Micropipettes containing SP and ACh were positioned in the right IML at the T2 level. Microinjection of threshold amounts of ACh (5 x 10(-2) M, 2-10 nl) and SP (3 x 10(-6) M, 2-10 nl) that caused small or no changes in HR or AP (less than 10 bpm or mmHg) elicited statistically significant synergistic increases in HR (22.9 +/- 3.3 bpm) but no changes in AP. Threshold microinjections of Glu (0.18 M, 2-10 nl) into the right RVLM combined with microinjections of threshold amounts of SP or ACh into the ipsilateral IML elicited significant synergistic increases in HR of 13.1 +/- 1.9 bpm and 10.6 +/- 1.9 bpm and in AP of 9.7 +/- 1.9 mmHg and 10.8 +/- 1.7 mmHg, respectively. These results indicate that SP and ACh interact to influence cardioacceleratory spinal preganglionic neurons (SPN) and interact with the transmitter released in the IML by RVLM stimulation to elicit increases in HR.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1991

Neuronal and cardiovascular responses to ANF microinjected into nucleus ambiguous.

Effects of microinjection of atrial natriuretic factor (ANF) into cardioinhibitory sites in the nucleus ambiguous (NA) or on single vagal cardioinhibitory neurons (VCN) were investigated in urethan-anesthetized rats. Sites containing cardioinhibitory neurons were identified by observing a marked and reproducible bradycardia in response to microiontophoretically applied (20-40 nA) or microinjected (20 nl) 0.1 M L-glutamate. In 35 of the 40 (87.5%) cardioinhibitory sites identified by microinjection of glutamate, ANF (20 nl of 10(-7) M) decreased heart rate (HR; -47.1 +/- 2.5 beats/min). No responses were elicited in the other five sites. In animals paralyzed and artificially ventilated, the HR effects of ANF were not significantly different before and after muscle paralysis. Microinjections of 10 nl of 10(-7) M ANF caused excitation of 19 of 21 VCN (90%), which was followed by a decrease in HR (-20.8 +/- 2.3 beats/min); no neuronal or cardiovascular responses were elicited by ANF in the remaining two VCN. Bilateral vagotomy or atropine sulfate (1 mg/kg iv) abolished cardiac slowing without affecting neuronal activation, whereas propranolol (2 mg/kg iv) did not affect either response to ANF. These results suggest that ANF is a neuromediator involved in the excitation of cardioinhibitory neurons in the NA.

Animals↗
PubMed1991

Interaction of putative transmitters in central nervous pathways involved in the control of heart rate and arterial pressure.

As many putative transmitter substances have been shown to be co-localized in areas of the central nervous system involved in cardiovascular control, we have investigated the possibility that some of these substances may interact in eliciting changes in heart rate and arterial pressure in anesthetized rats. In a first set of experiments, interactions between atrial natriuretic factor and glutamate were investigated by microinjection into the nucleus of the tractus solitarius, the site of termination of baroreceptor fibers of the aortic depressor nerve. In addition, interactions between the transmitter released in the nucleus tractus solitarius by electrical stimulation of the aortic depressor nerve and atrial natriuretic factor microinjected into the nucleus tractus solitarius were investigated. Combined microinjection of atrial natriuretic factor and glutamate into the nucleus tractus solitarius, or stimulation of the aortic depressor nerve combined with atrial natriuretic factor in the nucleus tractus solitarius, elicited decreases in heart rate and arterial pressure which were greater than the responses to either substance or stimulation alone or their algebraic sum. In a second set of experiments, interactions between substance P and acetylcholine were investigated in the intermediolateral nucleus of the spinal cord, the location of sympathetic preganglionic neurons. Furthermore, we investigated the possibility that the cardiovascular responses to microinjection of substance P and acetylcholine into the intermediolateral nucleus could be potentiated by the transmitter released in the intermediolateral nucleus by microinjection of glutamate into the rostral ventrolateral medulla, a region with known sympatho-excitatory function.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Catecholamines inhibit steroidogenesis by cultured porcine thecal cells.

The ovaries of many species contain catecholamines and beta-adrenergic receptors. The present studies were done to determine if catecholamines play a role in the regulation of androgen production by porcine theca cells. Basal and luteinizing hormone (LH)-stimulated androstenedione production was significantly inhibited by noradrenaline and isoproterenol. The inhibitory effects were dose-dependent and were enhanced when the cultures contained the carboxy-O-methyl transferase inhibitor, U-0521. The inhibitory effect of isoproterenol was reversed by the beta-adrenergic antagonist, metoprolol. Isoproterenol caused a generalized inhibition of LH-stimulated steroidogenesis, decreasing the accumulation of pregnenolone, progesterone, androstenedione and estradiol in the culture medium. These studies suggest that catecholamines may be important regulators of thecal androgen production.

Androstenedione↗
PubMed1990

Reciprocal connections between nucleus tractus solitarii and rostral ventrolateral medulla.

Experiments were done to test the hypothesis that there are reciprocal connections between the nucleus of the tractus solitarius (NTS) and the rostral ventrolateral medulla (RVLM). Spontaneous activity was recorded from units in the right RVLM or NTS of urethan-anesthetized and artificially ventilated rats. Twenty-four of 42 RVLM and 12 of 21 NTS units were classified as cardiovascular because they were inhibited by baroreceptor activation and displayed a cardiac rhythm. Electrical stimulation of depressor sites in the NTS inhibited 14 and excited 10 RVLM units. Stimulation of pressor sites in the RVLM excited 10 and inhibited 2 NTS units. None of the units in the NTS or in the EVLM could be activated antidromically. These results provide evidence that there are reciprocal excitatory and inhibitory connections between NTS and RVLM and that these connections are not monosynaptic.

Animals↗
PubMed1990

Site at which ovarian nerve extracts inhibit thecal androgen production.

We have recently reported that extracts of the superior ovarian nerve (SON) of rats inhibit porcine theca cell androstenedione production. Theca cells obtained from prepubertal gilts were cultured under serum-free conditions for 48 h. The inhibitory effect of SON extracts occurred within 6 h of treatment, was irreversible and independent of the dose of luteinizing hormone (LH) employed. The SON extracts' actions were exerted at a site(s) distal to the generation of adenosine 3',5'-monophosphate (cyclic AMP), since they did not affect extracellular cyclic AMP accumulation, while causing a significant inhibition of androstenedione production. The SON extract decreased 17 alpha-hydroxyprogesterone, androstenedione, testosterone, estradiol and estrone production while increasing progesterone and pregnenolone production, suggesting that the SON extract causes an inhibition of the 17 alpha-hydroxylase:C17-20 lyase complex. These results indicate that a factor(s) in the SON may play an important role in the regulation of follicular development, since thecal androgens are substrates for granulosa cell estrogen biosynthesis and are also involved in follicular atresia.

17-alpha-Hydroxyprogesterone↗
PubMed1990

Inhibition of rostral VLM by baroreceptor activation is relayed through caudal VLM.

Experiments were done to test the hypothesis that inhibition of neurons in the rostral ventrolateral medulla (RVLM) elicited by stimulation of the nucleus tractus solitarii (NTS) is relayed through the caudal ventrolateral medulla (CVLM). We recorded activity from 56 spontaneously firing units in the right RVLM of urethan-anesthetized and artificially ventilated rats. Eleven of these units were classified as cardiovascular neurons, because they were silenced by baroreceptor activation (1-3 micrograms phenylephrine iv) and showed rhythmicity of their spontaneous activity in synchrony with the cardiac cycle. Single pulses (0.1 ms, 30-75 microA) delivered 1/s to depressor sites in the ipsilateral NTS inhibited the activity of all these cardiovascular neurons. Microinjection of the glutamate antagonist kynurenic acid (0.15 M, 50 nl) into the ipsilateral CVLM blocked the inhibitory response of RVLM units to the administration of phenylephrine and increased the firing frequency of cardiovascular neurons in the RVLM by 43%. Moreover, kynurenic acid administration attenuated the inhibitory response of cardiovascular neurons in the RVLM to NTS stimulation. Finally, stimulation of the NTS that elicited depressor responses under control conditions produced a pressor response after kynurenic acid administration. The remaining 45 RVLM neurons were barosensitive but lacked cardiac cycle-related rhythmicity. These results provide direct evidence for the existence of a tonic inhibitory pathway from NTS to RVLM that is relayed through the CVLM probably by a glutamatergic projection from NTS to CVLM.

Animals↗
PubMed1990

Cardiovascular effects of microinjection of ANF and brain natriuretic peptide into ventrolateral medulla.

Cardiovascular effects of microinjection of atrial natriuretic factor (ANF) into 77 sites of the ventrolateral medulla (VLM) were investigated in urethan-anesthetized rats. Changes in mean arterial pressure (MAP) and heart rate (HR) in response to injections of glutamate into these sites were used to determine that they contained cardiovascular neurons. ANF (20 nl of 10(-7) M) decreased MAP [-8.9 +/- 1.5 (SE) mmHg] and HR [-9.0 +/- 2.8 (SE) beats/min] in 5 of 36 vasopressor sites identified by glutamate located in the more rostral and lateral aspect of the rostral VLM (RVLM); no effect was elicited in the other 31 RVLM sites. ANF decreased MAP (-10.4 +/- 2.4 mmHg) and HR (-9.8 +/- 3.0 beats/min) in 25 of 41 depressor sites distributed throughout the caudal VLM (CVLM); no response was observed in the other 16 CVLM sites. Brain natriuretic peptide (BNP) was microinjected (20 nl of 10(-7) M) in 21 VLM sites, before or after microinjection of ANF. BNP and ANF elicited similar results in 17 sites, a decline in MAP and HR in 10 sites, and no effect in 7 sites. In the remaining four cases ANF caused a decline in MAP and in HR, whereas BNP had minimal or no effect. Cardiovascular responses to ANF microinjection into the RVLM and CVLM support the hypothesis that ANF is involved in the transmission of baroreceptor information from the nucleus tractus solitarii to these medullary regions. The similarity of the results obtained with BNP and ANF suggests that these peptides may serve similar roles in medullary pathways involved in the control of the cardiovascular system.

Animals↗
PubMed1990

Microinjection of substance P and ACh into rat intermediolateral nucleus elicits cardiovascular responses.

The effects of substance P (SP) or acetylcholine (ACh) microinjected into the intermediolateral nucleus of the spinal cord (IMLn) on arterial pressure (AP) and heart rate (HR) were investigated in 22 male Wistar rats under urethan and artificial ventilation. L-Glutamate (Glu) was microinjected into the IMLn between C7 and T4 to locate cardiovascular sites. Micropipettes containing Glu were stereotaxically positioned in 82 histologically verified sites in the IMLn between C7 and T4 on both the right and left sides. Microinjection of 4-10 nl of 0.18 M Glu in 30 of 39 explored sites at the T2 level elicited significant increases in HR (+24.2 +/- 3.1 beats/min). These changes were accompanied by significant increases in mean AP (+11.4 +/- 1.2 mmHg) at the T2 level (32/47 sites). Microinjection of 4-10 nl of SP (3 X 10(-7) to 3 X 10(-4) M) or ACh (0.005-0.5 M) in the right IMLn at the T2 level elicited increases in HR but did not affect AP. The duration of the responses to SP or ACh was significantly longer than the duration of the responses to Glu. The responses to ACh could be blocked by prior microinjection of 5 X 10(-2) M atropine. No responses were ever obtained in the left IMLn by microinjection of Glu, SP, or ACh. These results support the hypothesis that Glu, ACh, and SP mediate sympathoexcitation in the IMLn of the rat and that these excitatory responses have different temporal patterns.

Acetylcholine↗
PubMed1989

Neurally mediated cardiovascular responses to stimulation of cell bodies in the hypothalamus of the rat.

To study the cardiovascular responses to selective activation of neuronal cell bodies in the hypothalamus, DL-homocysteate (5-50 nl of a 0.15-M solution, pH 7.4) was injected into 417 histologically verified sites in the hypothalamus of 46 urethan-anesthetized, paralyzed and artificially ventilated rats. Injections resulted in depressor responses (-5 to -32 mm Hg) in 271 sites, in pressor responses (5-47 mm Hg) in 77 sites and 69 sites were not responsive. Depressor effects had a shorter latency (85% started within 5 s) than pressor effects (42% started within 5 s). Control injections of 0.15 M NaCl into 126 of the responsive sites were ineffective. Arterial pressure (AP) responses showed a positive correlation (r = 0.61, P less than 0.001) with changes in heart rate (HR). Analysis of the anatomical distribution of responsive sites showed that in all hypothalamic subdivisions depressor responses predominated except in the paraventricular nucleus, where mainly pressor effects and tachycardia were elicited. These results demonstrate that excitation of cell bodies in most hypothalamic regions elicits neurally mediated changes in AP and HR and that the traditional functional division of the hypothalamus into a rostral depressor and a caudal pressor area is probably based on the combined excitation of fibers of passage and cell bodies.

Animals↗
PubMed1989

Cardiovascular responses and changes in neural activity in the rostral ventrolateral medulla elicited by electrical stimulation of the amygdala of the rat.

Electrical stimulation of the central nucleus of the amygdala (ACe) in anesthetized animals produces a decrease in arterial pressure (AP) as a result of an overall decrease in peripheral resistance. As the cardiovascular neurons that presumably mediate these changes are located in the rostral ventrolateral medulla (RVLM), we recorded spontaneous activity from 89 histologically verified units in the RVLM of urethan-anesthetized rats. Twenty-two of these units were classified as cardiovascular neurons because their spontaneous activity was inhibited by baroreceptor stimulation (2-4 micrograms phenylephrine i.v.) and displayed a cardiac cycle-related rhythmicity. Single or twin pulses (0.5 ms, 180 +/- 55 microA) delivered once per second to arterial depressor sites in the ipsilateral ACe inhibited the activity of 18 of these neurons and excited 4. In 27 additional barosensitive neurons that lacked cardiac cycle rythmicity, a similar distribution of effects was obtained by electrical stimulation of the ACe: 13 inhibited, 5 excited, 9 not affected. Finally, 40 non-barosensitive units were found; stimulation of the ACe inhibited the activity of 16, excited 12 and had not effect in 12. These results are interpreted to indicate that the differential effects of ACe stimulation on different vascular beds are mediated probably by differential influences on cardiovascular neurons in the RVLM, and that functions other than respiratory and cardiovascular control are represented in the RVLM.

Action Potentials↗
PubMed1989

Insulin enhances luteinizing hormone-stimulated steroidogenesis by porcine theca cells.

It has been shown recently that insulin enhances differentiation of rat, pig, and human granulosa cells. The present studies were done to determine if insulin also plays a role in the regulation of theca cell steroidogenesis. Theca cells were obtained from prepubertal gilts and cultured under serum-free conditions for 48 h. Theca cell androstenedione production under basal and luteinizing hormone (LH)-stimulated conditions was significantly increased by adding insulin (1 microgram/ml) to the culture medium. Treatment of basal and LH-stimulated cultures with increasing concentrations of insulin (0.001-10 micrograms/ml) caused dose- and time-dependent increments in androstenedione production, but the effect was independent of the dose of LH employed. The ability of insulin to enhance thecal cell androstenedione production was mimicked by somatomedin C, but not by relaxin. Studies to determine the mechanism(s) of action of insulin showed that insulin action is exerted, at least in part, at a site(s) proximal to cyclic adenosine 3'5'-monophosphate (cAMP) generation, since insulin enhanced both basal and LH-stimulated accumulation of extracellular cAMP in addition to increasing androstenedione production. This effect was further enhanced by 3-isobutyl-1-methyl xanthine, an inhibitor of phosphodiesterase activity. Insulin treatment also caused dose-dependent increments in forskolin- and prostaglandin E2-stimulated accumulation of extracellular cAMP and androstenedione. Insulin also increased both the basal and LH-stimulated production of progesterone and its precursor pregnenolone, in addition to the increases in androstenedione.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed1989

Catecholestrogens inhibit basal and luteinizing hormone-stimulated androgen production by porcine thecal cells.

It has been shown recently that catecholestrogens are produced by cultured porcine granulosa and thecal cells, and that they influence porcine granulosa cell steroidogenesis in a similar manner to estradiol-17 beta (E2). The present studies were performed to determine if catecholestrogens also play a role in the regulation of porcine thecal cell steroidogenesis and to compare their actions to those of E2. Thecal cells were obtained from prepubertal gilts and cultured in a serum-free medium for 48 h. Thecal cell androstenedione production under basal and luteinizing hormone (LH)-stimulated conditions was significantly inhibited by adding E2 or catecholestrogens to the culture medium. Treatment of basal and LH-stimulated cultures with increasing concentrations of E2 or catecholestrogens (0.1-10 micrograms/ml) caused a dose-and time-dependent inhibition of androstenedione production. The inhibitory effect of the catecholestrogens, but not of E2, was enhanced when the cultures contained the catechol-O-methyl transferase inhibitor, U-0521. Studies to determine the mechanism(s) of action of the catecholestrogens showed that E2 and catecholestrogen actions are exerted at a site(s) distal to cyclic adenosine 3'5' monophosphate (cyclic AMP) generation, because neither agent affected the basal or LH-stimulated accumulation of extracellular cyclic AMP, while causing a significant inhibition of androstenedione production. E2 or catecholestrogen treatment also inhibited androstenedione production stimulated by prostaglandin E2 and dibutyryl cyclic AMP. In addition, both E2 and catecholestrogen treatment significantly decreased basal and LH-stimulated 17 alpha-hydroxyprogesterone production, while significantly increasing pregnenolone production. Progesterone production in the presence of E2 or catecholestrogens showed small but statistically insignificant increases.(ABSTRACT TRUNCATED AT 250 WORDS)

17-alpha-Hydroxyprogesterone↗
PubMed1989

Neuronal and cardiovascular responses to ANF microinjected into the solitary nucleus.

The effect on single-unit activity, arterial pressure, and heart rate of a microinjection of atrial natriuretic factor (ANF) into 78 histologically verified sites in the nucleus tractus solitarii (NTS) was investigated in rats. Injections of 50 nl of 10(-7) M ANF excited 34 neurons (44%), mainly localized at the level of the obex, inhibited 15 (19%), and had no effect on the remaining 29 (37%). The increase in firing frequency of the 34 excited neurons was always followed by a decline in mean arterial pressure [MAP, -10.6 +/- 1.8 (SE) mmHg; P less than 0.01] and heart rate [HR, -9.6 +/- 3.1 (SE) beats/min; P less than 0.05]. When injections of ANF caused either no effect or inhibition of single-unit activity, no changes in either MAP or HR were observed. Single units excited by injections of ANF were also excited by activation of arterial baroreceptors and inhibited by baroreceptor unloading. Control injections of an inactive peptide analogue of ANF or of vehicle never produced any effects on neuronal firing frequency or on MAP and HR. Similar results were obtained from animals paralyzed and artificially ventilated. These results support the hypothesis that ANF plays a role in the chemical transmission of baroreceptor information within the NTS.

Animals↗
PubMed1989

Neurons in rostral VLM are inhibited by chemical stimulation of caudal VLM in rats.

Recent evidence suggests that neurons in the caudal ventrolateral medulla (CVLM) exert a tonic inhibition on the neurons in the rostral ventrolateral medulla (RVLM) that are essential for the maintenance of arterial pressure (AP). To test the hypothesis that selective activation of cell bodies in the CVLM can inhibit the discharge of neurons in the RVLM, activity from 88 neurons in the RVLM was recorded extracellularly while 2-30 nl sodium glutamate (Glu; 0.15 M) were microinjected into depressor sites of the CVLM of urethan-anesthetized male Wistar rats. Results obtained from spontaneously breathing and artificially ventilated rats were essentially similar and are presented together. Twenty-five neurons were characterized as cardiovascular because they were inhibited by baroreceptor activation and showed rhythmicity of their spontaneous activity in synchrony with the cardiac cycle. Activation of cell bodies in the CVLM inhibited the firing rate of 23 of these cardiovascular neurons and excited 2. The remaining 63 neurons could not be considered cardiovascular because they either were not barosensitive or lacked cardiac cycle-related rhythmicity. Injection of Glu into the CVLM inhibited 26 of these neurons, excited 22, and had no effect on 15. These results provide direct evidence for the existence of an inhibitory pathway from neurons located in the CVLM to cardiovascular neurons in the RVLM.

Animals↗
PubMed1989

Baroreceptor activation or glutamate coinjection facilitates depressor responses to ANF microinjection into NTS.

As microinjection of atrial natriuretic factor (ANF) into the nucleus of the solitary tract (NTS) has been shown to elicit depressor responses [D. J. McKitrick and F. R. Calaresu. Am. J. Physiol. 255 (Regulatory Integrative Comp. Physiol. 24): R182-R187, 1988], we investigated the possibility that these responses might be facilitated either by electrical stimulation of arterial baroreceptor fibers in the aortic depressor nerve (ADN) or by simultaneous microinjection of L-glutamate (Glu) into the same sites in the NTS. Male Wistar rats (n = 51) were anesthetized with urethan (1.4 g/kg ip), artificially ventilated, and the dorsal medulla was exposed. The ADN was isolated, cut distally, and the central end was placed on bipolar stimulating electrodes. Threshold doses of 10(-7) M ANF microinjected into the NTS were combined with threshold electrical stimulation of the ADN (n = 37) or threshold doses of 0.13-0.5 M Glu (n = 14) microinjected into the NTS. There was a significant interaction between ANF microinjection and ADN stimulation in producing changes in mean arterial pressure (MAP) and heart rate [HR; P less than 0.05; -20.2 +/- 2.3 (SE) mmHg and -30.8 +/- 6.9 (SE) beats/min, respectively; n = 18]. There was also a significant interaction between ANF and Glu in producing changes in MAP and HR [P less than 0.05; -16.3 +/- 1.8 (SE) mmHg and -15.0 +/- 3.0 (SE) beats/min, respectively; n = 8]. These results indicate that ANF influences neurons in the NTS, which are also influenced by activation of arterial baroreceptors, and ANF and Glu interact in the NTS to produce facilitated cardiovascular responses.

Animals↗