Reflex Changes in Sympathetic Activity and Arterial Blood Pressure Evoked by Afferent Stimulation of the Renal Nerve

1970 ◽  
Vol 78 (2) ◽  
pp. 184-188 ◽  
Author(s):  
H. Aars ◽  
S. Akre
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sympathetic Activity ◽  
Renal Nerve ◽  
Afferent Stimulation ◽  
Arterial Blood ◽  
Stimulation Of

scholarly journals Pharmacological assessment of the contribution of the arterial baroreflex to sympathetic discharge patterns in healthy humans

2018 ◽  
Vol 119 (6) ◽  
pp. 2166-2175 ◽  
Author(s):  
Jacqueline K. Limberg ◽  
Elizabeth P. Ott ◽  
Walter W. Holbein ◽  
Sarah E. Baker ◽  
Timothy B. Curry ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sympathetic Activity ◽  
High Threshold ◽  
Neural Activation ◽  
Afferent Activity ◽  
Cluster Number ◽  
Arterial Blood ◽  
Rate Coding ◽  
Low Threshold

To study how changes in baroreceptor afferent activity affect patterns of sympathetic neural activation, we manipulated arterial blood pressure with intravenous nitroprusside (NTP) and phenylephrine (PE) and measured action potential (AP) patterns with wavelet-based methodology. We hypothesized that 1) baroreflex unloading (NTP) would increase firing of low-threshold axons and recruitment of latent axons and 2) baroreflex loading (PE) would decrease firing of low-threshold axons. Heart rate (HR, ECG), arterial blood pressure (BP, brachial catheter), and muscle sympathetic nerve activity (MSNA, microneurography of peroneal nerve) were measured at baseline and during steady-state systemic, intravenous NTP (0.5–1.2 µg·kg−1·min−1, n = 13) or PE (0.2–1.0 µg·kg−1·min−1, n = 9) infusion. BP decreased and HR and integrated MSNA increased with NTP ( P < 0.01). AP incidence (326 ± 66 to 579 ± 129 APs/100 heartbeats) and AP content per integrated burst (8 ± 1 to 11 ± 2 APs/burst) increased with NTP ( P < 0.05). The firing probability of low-threshold axons increased with NTP, and recruitment of high-threshold axons was observed (22 ± 3 to 24 ± 3 max cluster number, 9 ± 1 to 11 ± 1 clusters/burst; P < 0.05). BP increased and HR and integrated MSNA decreased with PE ( P < 0.05). PE decreased AP incidence (406 ± 128 to 166 ± 42 APs/100 heartbeats) and resulted in fewer unique clusters (15 ± 2 to 9 ± 1 max cluster number, P < 0.05); components of an integrated burst (APs or clusters per burst) were not altered ( P > 0.05). These data support a hierarchical pattern of sympathetic neural activation during manipulation of baroreceptor afferent activity, with rate coding of active neurons playing the predominant role and recruitment/derecruitment of higher-threshold units occurring with steady-state hypotensive stress. NEW & NOTEWORTHY To study how changes in baroreceptor afferent activity affect patterns of sympathetic neural activation, we manipulated arterial blood pressure with intravenous nitroprusside and phenylephrine and measured sympathetic outflow with wavelet-based methodology. Baroreflex unloading increased sympathetic activity by increasing firing probability of low-threshold axons (rate coding) and recruiting new populations of high-threshold axons. Baroreflex loading decreased sympathetic activity by decreasing the firing probability of larger axons (derecruitment); however, the components of an integrated burst were unaffected.

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

Mechanisms of action of sodium cromoglycate

1985 ◽  
Vol 63 (6) ◽  
pp. 760-765 ◽  
Author(s):  
D. F. Biggs ◽  
V. Goel
Keyword(s):  
Blood Pressure ◽  
Sodium Cromoglycate ◽  
Arterial Blood Pressure ◽  
Vagal Stimulation ◽  
Cardiovascular Responses ◽  
Bilateral Stimulation ◽  
Vagus Nerves ◽  
Arterial Blood ◽  
Efferent Pathways ◽  
Stimulation Of

The effects of sodium cromoglycate (SCG) on cardiovascular and pulmonary responses to phenylbiguanide, capsaicin, and vagal stimulation were studied in anesthetized guinea pigs. Phenylbiguanide had no bronchospastic activity but induced reflex changes in arterial blood pressure which were reduced or abolished by SCG. Capsaicin induced nonreflex bronchospasm, and decreases in arterial blood pressure that were unaffected by SCG. Sodium cromoglycate, given before or after atropine, had no effect on the bronchospasm and cardiovascular responses to unilateral or bilateral stimulation of the vagus nerves. We conclude that SCG may influence both the afferent and efferent pathways of responses to drugs.

Beta2-mediated hypotension and myocardial injury

1982 ◽  
Vol 60 (8) ◽  
pp. 1144-1148 ◽  
Author(s):  
Alison Brown-Lukacsko ◽  
Peter Lukacsko
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Myocardial Injury ◽  
Elevated Serum ◽  
Blocking Agent ◽  
Arterial Blood ◽  
Ganglionic Blocking ◽  
Elevated Heart Rate ◽  
Stimulation Of

This study was designed to investigate the importance of beta2 receptor mediated hypotension in the pathogenesis of myocardial injury. The effect of isoproterenol and the putative beta2 agonist albuterol on arterial blood pressure, heart rate, the myocardial content of ATP and cAMP, and the serum content of MB-CPK was examined in conscious rats. Isoproterenol (5.25 mg/kg, s.c.) and albuterol (45 mg/kg, s.c.) lowered blood pressure and elevated heart rate to the same extent. Also, both agonists increased the myocardial content of cAMP, decreased the myocardial content of ATP, and elevated serum MB-CPK. The beta1 antagonist practolol, but not the ganglionic blocking agent chlorisondamine, attenuated the elevation in heart rate to albuterol without reducing its effect on blood pressure. Practolol, but not chlorisondamine, abolished the effects of albuterol on cAMP, ATP, and MB-CPK. These data suggest that the myocardial injury which is associated with an increased heart rate and changes in cAMP, ATP, and MB-CPK following the administration of albuterol is not the result of beta2-mediated hypotension, but is due to stimulation of myocardial beta1 receptors.

Cerebral blood flow and behavior during brain stimulation in the goat

1977 ◽  
Vol 232 (5) ◽  
pp. H495-H499
Author(s):  
M. Manrique ◽  
E. Alborch ◽  
J. M. Delgado
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Maxillary Artery ◽  
Internal Maxillary Artery ◽  
Arterial Blood ◽  
And Behavior ◽  
Stimulation Of

Cerebral blood flow, heart rate, arterial blood pressure, and behavior were studied in conscious goats during electrical stimulation of the diencephalon and mesencephalon. Stimulation of the subthalamic area produced a considerable increase in ipsilateral cerebral blood flow and heart rate, accompanied by either a small or a large increase in systemic arterial blood pressure. Cardiovascular effects were associated with changes in alertness. The increase in cerebral blood flow was partially abolished by previous administration of atropine directly into the internal maxillary artery. Stimulation of the mesencephalic reticular formation caused a marked increase in blood pressure with no change or with some decrease in cerebral blood flow. After administration of phentolamine into the internal maxillary artery, stimulation produced increase in cerebral blood flow. The behavioral response consisted of restlessness and attempted flight. These results suggest the existence of cholinergic vasodilator and adrenergic vasoconstrictor pathways to cerebral blood vessels that may be stimulated electrically.

Bradykinin in reflex cardiovascular responses to static muscular contraction

1986 ◽  
Vol 61 (1) ◽  
pp. 271-279 ◽  
Author(s):  
C. L. Stebbins ◽  
J. C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Response ◽  
Time Derivative ◽  
Cardiovascular Responses ◽  
Carboxypeptidase B ◽  
Arterial Blood ◽  
Static Contraction ◽  
Stimulation Of

We examined the contribution of bradykinin to the reflex hemodynamic response evoked by static contraction of the hindlimb of anesthetized cats. During electrical stimulation of ventral roots L7 and S1, we compared the cardiovascular responses to hindlimb contraction before and after the following interventions: inhibition of converting enzyme (kininase II) with captopril (3–4 mg/kg, n = 6); inhibition of kallikrein activity with aprotinin (Trasylol, 20,000–30,000 KIU/kg, n = 8); and injection of carboxypeptidase B (500–750 U/kg, n = 7). Treatment with captopril augmented the rise in mean arterial blood pressure and maximal time derivative of pressure (dP/dt) caused by static contraction from 21 +/- 3 to 39 +/- 7 mmHg and 1,405 +/- 362 to 2,285 +/- 564 mmHg/s, respectively. Aprotinin attenuated the contraction-induced rise in mean arterial blood pressure (28 +/- 4 to 9 +/- 2 mmHg) and maximal dP/dt (1,284 +/- 261 to 469 +/- 158 mmHg/s). Carboxypeptidase B reduced the cardiovascular response to static contraction. Thus the mean arterial blood pressure response was decreased from 36 +/- 12 to 24 +/- 11 mmHg, maximal dP/dt from 1,618 +/- 652 to 957 +/- 392 mmHg/s, and heart rate from 12 +/- 2 to 7 +/- 1 beats/min. These data suggest that stimulation of muscle afferents by bradykinin contributes to a portion of the reflex cardiovascular response to static contraction.

PREFERENTIAL RELEASE OF OXYTOCIN FROM THE NEUROHYPOPHYSIS AFTER ELECTRICAL STIMULATION OF THE AFFERENT PATH OF THE MILK-EJECTION REFLEX IN THE BRAIN OF THE GUINEA-PIG

1968 ◽  
Vol 40 (2) ◽  
pp. 205-214 ◽  
Author(s):  
J. S. TINDAL ◽  
G. S. KNAGGS ◽  
A. TURVEY
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Guinea Pig ◽  
Arterial Blood Pressure ◽  
Pituitary Stalk ◽  
Milk Ejection ◽  
Arterial Blood ◽  
Milk Ejection Reflex ◽  
The Brain ◽  
Stimulation Of

SUMMARY Discrete portions of the afferent path of the milk-ejection reflex have been explored in the brain of the lactating guinea-pig. Both intramammary pressure and arterial blood pressure were recorded to detect release of oxytocin and vasopressin. It was found that the milk-ejection responses which occurred after electrical stimulation of the pathway in the midbrain and hypothalamus were caused by the release of oxytocin without detectable release of vasopressin. A mixture of oxytocin and vasopressin, in the ratio of approximately 3:1, was released only after electrical stimulation of the rostral tuberal region of the hypothalamus adjacent to the pituitary stalk. It is concluded that the afferent path in the brain of the guinea-pig studied is concerned with the preferential release of oxytocin from the neurohypophysis and that it is the pathway of the milk-ejection reflex.

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