The Action of L(-)-Dopa on Baroreflexes in Parkinsonism

1972 ◽  
Vol 43 (6) ◽  
pp. 851-859 ◽  
Author(s):  
J. L. Reid ◽  
D. B. Calne ◽  
C. F. George ◽  
S. D. Vakil
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Horizontal Position ◽  
Postural Change ◽  
Arterial Blood ◽  
Cardiovascular Reflex ◽  
Significant Impairment ◽  
The Central Nervous System ◽  
Valsalva's Manoeuvre ◽  
Blood Pressure Responses

1. The intra-arterial blood pressure responses to Valsalva's manoeuvre and postural change were investigated as indices of cardiovascular reflex activity in seventeen Parkinsonian patients on maximally tolerated doses of l(-)-dopa (levodopa) and repeated in nine patients on levodopa with an extracerebral decarboxylase inhibitor, l-alpha methyldopahydrazine. The results were compared with control pretreatment responses. 2. There was significant impairment of the pressor response to Valsalva's manoeuvre on levodopa, which returned to control values after the addition of l-alpha methyldopahydrazine. 3. The systolic, diastolic and mean arterial pressures measured in a horizontal position during treatment with levodopa, with and without l-alpha methyldopahydrazine, were significantly lower than pretreatment values. 4. It is concluded that the impairment of baroreflex function by levodopa is mediated, at least in part, at the periphery. In contrast, mechanisms operating within the central nervous system contribute to the lowering of blood pressure recorded in the horizontal position in patients receiving levodopa.

Role of NO on vasopressin and oxytocin release and blood pressure responses during osmotic stimulation in rats

1997 ◽  
Vol 273 (3) ◽  
pp. R1024-R1030 ◽  
Author(s):  
M. Kadekaro ◽  
H. Liu ◽  
M. L. Terrell ◽  
S. Gestl ◽  
V. Bui ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
No Synthase ◽  
Arterial Blood ◽  
Artificial Cerebrospinal Fluid ◽  
Osmotic Stimulation ◽  
Oxytocin Release ◽  
Enhanced Secretion ◽  
Blood Pressure Responses ◽  
Needle Prick

NG-nitro-L-arginine methyl ester (L-NAME, 250 micrograms/5 microliters), an inhibitor of nitric oxide (NO) synthase, or artificial cerebrospinal fluid (5 microliters) was administered intracerebroventricularly to conscious naive rats or to rats treated subcutaneously (15 microliters/kg) with NaCl (0.15, 0.45, or 1.0 M) or given a needle prick only. Intracerebroventricular injection of L-NAME increased plasma concentration of vasopressin (VP) and oxytocin (OT) in control naive rats, indicating that NO tonically inhibits basal secretion of both hormones during isosmotic isovolemic conditions. Osmotic stimulation with hypertonic saline (0.45 and 1.0 M NaCl) elevated plasma levels of both hormones as expected. Central blockade of NO synthase further enhanced secretion of OT during mild, but not strong, osmotic stimulation, whereas the high levels of VP remained unaffected by L-NAME. In animals treated with the needle prick or 0.15 M NaCl, only OT levels were increased after L-NAME. Therefore, NO selectively inhibits OT release in response to a painful stimulus (needle prick) and moderate osmotic stimulation to promote a preferential release of VP. A transient pressor response was observed after subcutaneous injection of 0.15 and 0.45 M NaCl, but a sustained response was obtained after 1.0 M NaCl. Regardless of whether the animals received NaCl solutions, however, treatment with L-NAME elevated blood pressure in all animals. Thus NO-induced vasodilation maintains basal arterial blood pressure and limits the pressor response to osmotic stimulation.

Effects of PNF Stretching Phases on Acute Arterial Blood Pressure

1995 ◽  
Vol 20 (2) ◽  
pp. 222-229 ◽  
Author(s):  
William L. Cornelius ◽  
Randall L. Jensen ◽  
Michael E. Odell
Keyword(s):  
Blood Pressure ◽  
Range Of Motion ◽  
Pressor Response ◽  
Maximal Voluntary Isometric Contraction ◽  
Concentric Contraction ◽  
Arterial Blood ◽  
Group 2 ◽  
Blood Pressure Responses ◽  
Hip Flexion ◽  
Passive Stretch

This study examined acute systolic (SBP) and diastolic (DBP) blood pressure responses within passive and modified proprioceptive neuromuscular facilitation (PNF) stretching techniques. Nonhypertensives (N = 60) were assigned to one of three treatment groups. Group 1 employed an antagonist passive stretch (APS), 6-sec maximal voluntary isometric contraction (MVIC) of the antagonist, and subsequent APS. Group 2 employed an APS, a 6-sec MVIC of the antagonist, submaximal concentric contraction of the agonist, and APS. Group 3 was similar to Group 2, with the deletion of an MVIC prior to the concentric contraction. Blood pressures were obtained during rest, baseline following passive stretch, and at the end of the three phases of the PNF technique. Range of motion (ROM) data were collected for baseline and treatment in terminal hip flexion for each group. All PNF treatments were effective for increasing ROM. One or two trials of PNF improve ROM and avoid increasing SBP, while a third trial increases SBP. Key words: flexibility, nonhypertensives, pressor response, range of motion

Naloxone reverses inhibitory effect of electroacupuncture on sympathetic cardiovascular reflex responses

1999 ◽  
Vol 276 (6) ◽  
pp. H2127-H2134 ◽  
Author(s):  
Dong M. Chao ◽  
Lin L. Shen ◽  
Stephanie Tjen-A-Looi ◽  
Koullis F. Pitsillides ◽  
Peng Li ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Inhibitory Effect ◽  
Reflex Response ◽  
Ventrolateral Medulla ◽  
Arterial Blood ◽  
Cardiovascular Reflex ◽  
Wide Range ◽  
Feline Model ◽  
Stimulation Of

Acupuncture and electroacupuncture (EA) have been used in traditional Chinese medicine to treat a wide range of diseases and conditions, including angina pectoris and myocardial infarction. In a feline model of reflex-induced reversible myocardial ischemia, electrical stimulation of the median nerves to mimic EA (Neiguan acupoint) significantly improved ischemic dysfunction, secondary to an inhibitory effect of EA on reflex pressor effects evoked by bradykinin (BK). The central mechanism of EA’s inhibitory effect in this model is unknown. Accordingly, in α-chloralose-anesthetized cats, BK (10 μg/ml) was applied to the gallbladder to elicit a cardiovascular reflex response that significantly ( P < 0.05) increased arterial blood pressure and heart rate; normalized systolic wall thickening (%WTh) of the left ventricle, measured by ultrasonic single-crystal sonomicrometer, increased by 31 ± 11% ( P < 0.05). After ligation of a side branch of the left anterior descending coronary artery, the reflex pressor response to BK resulted in a significant decrease of %WTh (−32 ± 6%) in the ischemic region. When bilateral EA of the Neiguan acupoints was performed, the pressor response to BK was inhibited and regional myocardial function was significantly improved (+19 ± 20%). The inhibitory effects of EA on blood pressure and %WTh were reversed by intravenous injection of naloxone (0.4 mg/kg; n = 9) or microinjection of naloxone (10 nM in 0.1 μl/site; n= 14) into the rostral ventrolateral medulla (rVLM). Thus %WTh with intravenous naloxone was reduced to −13 ± 29% ( P<0.05) during stimulation of the gallbladder. Our results indicate that the inhibitory effect of EA on the BK-induced pressor response and the consequent improvement of ischemic dysfunction is dependent on the activation of opioid receptors, specifically receptors located in the rVLM.

Blood pressure during routine activity, stress, and feeding in black racer snakes (Coluber constrictor)

1993 ◽  
Vol 264 (1) ◽  
pp. R79-R84 ◽  
Author(s):  
J. N. Stinner ◽  
D. L. Ely
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Acute Stress ◽  
Pressor Response ◽  
Routine Activity ◽  
Plasma Norepinephrine ◽  
Arterial Blood ◽  
Coluber Constrictor ◽  
S Peak ◽  
Hematological Changes

The pressor response to normal daily behaviors and acute stress was studied in black racer snakes (Coluber constrictor) at 30 degrees C. In addition, hematological changes during the stress response were assessed. Mean nighttime systemic arterial blood pressure (SABP) in undisturbed snakes was lower than daytime pressure (26 +/- 3 vs. 32 +/- 9 mmHg, P < 0.001). When snakes were fed mice, SABP increased 3.5- to 4-fold and heart rate increased approximately 3-fold above resting values within approximately 30 s (peak SABP, 99 +/- 18 mmHg; peak heart rate, 99 +/- 12 beats/min). Killing and ingesting the mice required 6-15 min, during which time mean SABP and heart rate were 84 +/- 16 mmHg and 92 +/- 12 beats/min. Pulmonary blood pressure also increased but remained 40-50 mmHg lower than SABP. During stress elicited by tapping the snakes for 5-8 min, heart rate was 94 +/- 6 beats/min but SABP averaged only 44 +/- 11 mmHg. Plasma norepinephrine and epinephrine increased 51- and 26-fold. Plasma glucose increased 58%, hematocrit increased 19%, and plasma volume decreased 19%. It is concluded that blood pressure is markedly affected by behavior and that the sympathetic nervous system appears to play a key role.

Cardiovascular and neuroendocrine responses to baroreceptor denervation in baboons

1990 ◽  
Vol 258 (4) ◽  
pp. R930-R938 ◽  
Author(s):  
R. E. Shade ◽  
V. S. Bishop ◽  
J. R. Haywood ◽  
C. K. Hamm
Keyword(s):  
Blood Pressure ◽  
Aortic Arch ◽  
Carotid Sinus ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Plasma Norepinephrine ◽  
Arterial Blood ◽  
Bilateral Carotid ◽  
Vasopressin Secretion ◽  
Blood Pressure Responses

The purpose of this study was to describe the hormonal and blood pressure responses to partial (carotid sinus) and complete (carotid sinus + aortic arch) baroreceptor denervation in baboons. Experiments were performed in eight adult male baboons maintained on a tether system for the continuous measurement of mean arterial blood pressure (MAP) and heart rate (HR). Bilateral carotid sinus denervation (CSD) immediately increased MAP from 83 +/- 2.2 to 124 +/- 7.3 mmHg. MAP gradually decreased over the next 14 days to intact levels. There were also transient decreases in HR variability and increases in blood pressure variability after CSD. Subsequent denervation of the aortic arch to produce sinoaortic denervation (SAD) resulted in another abrupt large increase in MAP followed by a small but significant increase in MAP of 11 mmHg that was maintained for up to 4 wk after SAD. The short-term variability of HR and blood pressure was chronically decreased and increased, respectively, after SAD. Plasma renin activity, vasopressin, and epinephrine were not changed from intact levels either after CSD or SAD. Plasma norepinephrine was only transiently increased by CSD and chronically elevated by 72% over intact levels after SAD. Thus CSD in the baboon does not produce a sustained increase in MAP. SAD chronically increases MAP and is associated with evidence for an increased sympathetic tone. There is no indication that either increased renin secretion or vasopressin secretion contributes to the chronic cardiovascular effects of SAD in baboons.

Interaction of bradykinin and prostaglandin E1 on cardiac pressor reflex and sympathetic afferents

1986 ◽  
Vol 250 (5) ◽  
pp. R815-R822 ◽  
Author(s):  
T. Nerdrum ◽  
D. G. Baker ◽  
H. M. Coleridge ◽  
J. C. Coleridge
Keyword(s):  
Blood Pressure ◽  
Prostaglandin E1 ◽  
Pressor Response ◽  
Interactive Effect ◽  
Small Reduction ◽  
Arterial Blood ◽  
Repeated Applications ◽  
Pressor Reflex ◽  
Cardiac Afferents ◽  
Afferent Response

Bradykinin applied to the epicardium stimulates cardiac sympathetic afferents and evokes a reflex increase in arterial blood pressure. In anesthetized cats we examined the potentiation of these effects by prostaglandin E1 (PGE1) applied to the ventricular epicardium. We recorded cardiac afferent impulses from the second to the fifth left thoracic sympathetic rami. PGE1 (0.1 microgram/ml) alone had little effect on blood pressure, but it significantly increased the pressor response to bradykinin, and it reduced or abolished tachyphylaxis to repeated applications of bradykinin. Both mechanosensitive and chemosensitive sympathetic cardiac afferents were stimulated by bradykinin. Indomethacin (intravenous) caused a small reduction in the afferent response to bradykinin. Epicardial application of PGE1 significantly increased the response (magnitude and duration) of chemosensitive endings to bradykinin but not that of mechanosensitive endings; however, PGE1 abolished the tachyphylaxis of both chemosensitive and mechanosensitive endings to repeated applications of bradykinin. Because both bradykinin and prostaglandins are released in the ischemic myocardium, their interactive effect on cardiac sympathetic afferents could play a part in the sensory and reflex responses to myocardial ischemia.

Vasodepressor action of angiotensin in conscious chickens

1982 ◽  
Vol 243 (3) ◽  
pp. H456-H462 ◽  
Author(s):  
Y. Nakamura ◽  
H. Nishimura ◽  
M. C. Khosla
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Direct Action ◽  
Angiotensin Receptors ◽  
Ang Ii ◽  
Prostaglandin Synthetase ◽  
Vasopressin Antagonist ◽  
Native Chicken ◽  
Blood Pressure Responses ◽  
Depressor Action

In chronically cannulated conscious chickens, Gallus gallus, native chicken angiotensin II ([Asp1,Val5]ANG II) caused biphasic blood pressure responses, a depressor followed by a pressor response. The pressor response appears to be mediated primarily by catecholamines. The depressor responses increased with increasing doses and were accompanied by tachycardia. The onset of the depressor action of [Asp1,Val5]ANG II (2.49 +/- 0.22 s) was nearly as quick as that of acetylcholine or histamine. Replacement of aspartic acid in position 1 with sarcosine or asparagine reduced both depressor and pressor potencies, whereas there was no difference either in depressor or pressor potencies between [Asp1,Val5] and [Asp1,Ile5]ANG II. The depressor response to [Asp1,Val5]ANG II was not inhibited by atropine, a vasopressin antagonist, prostaglandin synthetase inhibitors, methysergide, or propranolol but was blocked markedly by [Sar1, Ile8]ANG II and partially by [Sar1,Thr8]ANG II. The results suggest that the vasodepressor action of ANG II is mediated by angiotensin receptors and may possibly be a direct action on the vascular smooth muscle.

Sex differences in central adrenoreceptor-mediated vasopressin response to hemorrhage

1991 ◽  
Vol 260 (5) ◽  
pp. E780-E786 ◽  
Author(s):  
J. D. Stone ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Sex Differences ◽  
Mean Arterial Blood Pressure ◽  
Intracerebroventricular Injection ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Blood Pressure Responses ◽  
Induced Changes

Hemorrhage-induced changes in the plasma vasopressin concentration and mean arterial blood pressure (MABP) were studied in conscious rats of both sexes with and without central alpha 1-adrenoreceptor blockade. Rats were subjected to two sequential hemorrhages (H1 and H2), each 0.8% of body weight after an intracerebroventricular injection of the alpha 1-adrenoreceptor antagonist corynanthine or of vehicle. H1 stimulated vasopressin secretion more in proestrous females than in males; there were no significant sex-related differences in responses to H2. Corynanthine pretreatment attenuated the vasopressin response to H2 in males, potentiated this response in proestrous females, but had no effect in estrous females. MABP decreased after H1 in all female groups and in corynanthine-pretreated males. After H2, all groups were hypotensive to the same extent. These data indicate that central alpha 1-adrenoreceptor-mediated pathways participate in vasopressin and blood pressure responses to hemorrhage, but their role is complex and is dependent on gender and on the phase of the estrous cycle.

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