scholarly journals Urine from Sexually Mature Intact Male Mice Contributes to Increased Cardiovascular Responses during Free-Roaming and Restrained Conditions

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Dexter L. Lee ◽  
Justin L. Wilson

Pheromones in the urine regulate aggression of male mice and castrated males produce less of these pheromones. We tested the hypothesis that pheromones in the urine of sexually mature-intact (SMI) males placed in the cage bedding of an individually housed male mouse or in a mouse restrainer would contribute to a significant increase in mean arterial pressure (MAP), heart rate (HR), and activity. Sexually mature male C57BL/6 mice were implanted with a biotelemetry transmitter to measure MAP, HR, and activity. Urine (200 μL) from SMI mice placed in the cages of singularly housed male mice caused significant changes above baseline values for MAP (21±4 mmHg), HR (145±25 bpm), and activity (9±2 counts) when compared to urine from castrated mice-induced MAP (11±3 mmHg), HR (70±15 bpm), and activity (5±1 counts). Pretreatment with terazosin significantly reduced the change in MAP (9±3 mmHg), heart rate (90±15 bpm), and activity (4±2 counts) responses to urine from SMI males. Saline did not significantly increase MAP, HR, or activity in any group. During restraint, urine from SMI mice caused a significant change in MAP (5±0.4 mmHg) and HR (17±1 bpm); urine from castrated mice did not cause a significant increase in MAP and HR. Our results demonstrate that a significant increase in MAP, HR, and activity occurs when male mice are exposed to urine pheromones from SMI males. In summary, pheromones in the urine of SMI male excreted in the cage bedding and mouse restrainers contribute to a significant increase in cardiovascular responses in the absence of direct physical contact with a different male mouse or animal handler.

2007 ◽  
Vol 292 (2) ◽  
pp. R937-R945 ◽  
Author(s):  
Orville A. Smith ◽  
Cliff A. Astley

Hypertension is a prominent underlying factor in the genesis of cardiovascular-related morbidity and mortality. A major impediment to the investigation into the causes of the disease is the paucity of naturally occurring animal models of the disease. There is evidence that some species of New World primates spontaneously become hypertensive. We used chronically implanted pressure transducers to assess normally occurring blood pressure and heart rate levels at rest and during routine laboratory procedures in a group of one of these New World primates ( Aotus sp.). Resting mean arterial pressure ranged from 72 to 130 mmHg. Three animals were judged to have resting mean arterial pressure levels in the hypertensive range (≥110 mmHg). In all of the animals, pressor responses to routine laboratory events were exaggerated (average highest mean pressure during 1 min from any session was 97–196 mmHg). Subsequently, the region of the perifornical/lateral hypothalamus known to produce elevated blood pressure and heart rate responses to electrical stimulation was removed, and the blood pressure responses to the laboratory routines were significantly decreased and, in some cases, eliminated. Control lesions in nearby tissue had no effect on these responses. This region may play a critical role in initiating or exacerbating cardiovascular responses that contribute to the development of essential hypertension.


1989 ◽  
Vol 256 (2) ◽  
pp. R577-R582 ◽  
Author(s):  
R. Ermirio ◽  
P. Ruggeri ◽  
C. E. Cogo ◽  
C. Molinari ◽  
F. R. Calaresu

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.


1989 ◽  
Vol 256 (6) ◽  
pp. R1340-R1347 ◽  
Author(s):  
T. Kitanaka ◽  
R. D. Gilbert ◽  
L. D. Longo

To determine the maternal cardiovascular responses to long-term hypoxemia, we studied three groups of animals: 1) pregnant ewes (n = 20) at 110-115 days gestation subjected to hypoxia for up to 28 days; 2) pregnant ewes (n = 4) that served as normoxic controls; and 3) nonpregnant ewes (n = 6) subjected to hypoxemia for up to 28 days. We measured mean arterial pressure, heart rate, uterine blood flow, and uterine vascular resistance continuously for 1 h/day while the ewe was exposed to an inspired O2 fraction of 12-13% for at least 17 days. Arterial PO2, O2 saturation, hemoglobin, arteriovenous O2 difference, and uterine O2 uptake were measured daily while blood volume and erythropoietin concentration were measured weekly. In the pregnant hypoxic group arterial PO2 decreased from a control value of 101.5 +/- 5.1 to 59.2 +/- 5.1 Torr within a few minutes, where it remained throughout the study. The hemoglobin concentration increased from 8.9 +/- 0.5 to 10.0 +/- 0.5 g/dl within 24 h where it remained, whereas erythropoietin concentration increased from 16.6 +/- 2.1 to 39.1 +/- 7.8 mU/ml at 24 h but then returned to near-control levels. Arterial glucose concentration, mean arterial pressure, and cardiac output decreased slightly but insignificantly. In contrast, body weight, heart rate, blood volume, uterine blood flow, uterine O2 flow, uteroplacental O2 uptake, and the concentrations of catecholamines and cortisol remained relatively constant. Thus both pregnant and nonpregnant sheep experience relatively minor cardiovascular and hematologic responses in response to long-term hypoxemia of moderate severity.


1987 ◽  
Vol 65 (11) ◽  
pp. 2182-2187 ◽  
Author(s):  
Harout Hasséssian ◽  
Réjean Couture ◽  
Line Jacques

In urethane-anaesthetized rats, the intrathecal administration of 6.5 nmol of substance P (SP), neurokinin A (NKA), or neurokinin B (NKB) at the T8–T10 level of the spinal cord enhances mean arterial pressure and heart rate. However, in the pentobarbital-anaesthetized rat, while NKB produces no effect on mean arterial pressure, NKA produces a biphasic change and SP, a depressor response. All three neurokinins elicit a tachycardia. The following rank order of potency SP ≥ NKA > NKB is observed in relation to these cardiovascular responses when either one of the two anaesthetics is used. The low cardiovascular activity of NKB cannot be attributed to its hydrophobicity, as the water soluble analogue of NKB, [Arg0] NKB, elicits a response as weak as the native peptide. In pentobarbital-anaesthetized rats, the intrathecal administration of 6.5 nmol of SP, also enhances plasma protein extravasation in cutaneous tissues of the back, the hind paws, and the ears. In this response NKA and NKB are either inactive (skin of hind paws) or less potent than SP (ears and dorsal skin). These findings agree with the hypothesis that in the rat spinal cord, the neurokinin receptor producing changes in mean arterial pressure, heart rate, and vascular permeability is of the NK-1 subtype.


2004 ◽  
Vol 286 (1) ◽  
pp. R138-R142 ◽  
Author(s):  
Ulrich Nordheim ◽  
Karl G. Hofbauer

In the present experiments the gut hormone peptide YY3-36 (PYY3-36), which inhibits neuropeptide Y (NPY) release, was used as a tool to study the cardiovascular effects of endogenous NPY under different dietary regimens in rats instrumented with a telemetry transmitter. In a first experiment, rats were placed on a standard chow diet ad libitum and in a second experiment on a high-fat diet ad libitum. After 6 wk, PYY3-36 (300 μg/kg) or vehicle was injected intraperitoneally. In a third experiment, PYY3-36 or vehicle was administered after 14 days of 50% restriction of a standard chow diet. In food-restricted rats, PYY3-36 increased mean arterial pressure (7 ± 1 mmHg, mean ± SE, P < 0.001 vs. saline, 1-way repeated-measures ANOVA with Bonferroni t-test) and heart rate (22 ± 4 beats/min, P < 0.001) during 3 h after administration. Conversely, PYY3-36 did not influence mean arterial pressure (0 ± 1 mmHg) and heart rate (-8 ± 5 beats/min) significantly in rats on a high-fat diet. Rats fed standard chow diet ad libitum showed an intermediate response (mean arterial pressure 4 ± 1 mmHg, P < 0.05, and heart rate 5 ± 2 beats/min, not significant). Thus, in our studies, divergent cardiovascular responses to PYY3-36 were observed in rats on different dietary regimens. These findings suggest that the cardiovascular effects of PYY3-36 depend on the hypothalamic NPY release, which is increased after chronic food restriction and decreased during a high-fat diet.


Cephalalgia ◽  
2019 ◽  
Vol 40 (3) ◽  
pp. 266-277
Author(s):  
Willebrordus PJ van Oosterhout ◽  
Guus G Schoonman ◽  
Dirk P Saal ◽  
Roland D Thijs ◽  
Michel D Ferrari ◽  
...  

Introduction Migraine and vasovagal syncope are comorbid conditions that may share part of their pathophysiology through autonomic control of the systemic circulation. Nitroglycerin can trigger both syncope and migraine attacks, suggesting enhanced systemic sensitivity in migraine. We aimed to determine the cardiovascular responses to nitroglycerin in migraine. Methods In 16 women with migraine without aura and 10 age- and gender-matched controls without headache, intravenous nitroglycerin (0.5 µg·kg−1·min−1) was administered. Finger photoplethysmography continuously assessed cardiovascular parameters (mean arterial pressure, heart rate, cardiac output, stroke volume and total peripheral resistance) before, during and after nitroglycerin infusion. Results Nitroglycerin provoked a migraine-like attack in 13/16 (81.2%) migraineurs but not in controls ( p = .0001). No syncope was provoked. Migraineurs who later developed a migraine-like attack showed different responses in all parameters vs. controls (all p < .001): The decreases in cardiac output and stroke volume were more rapid and longer lasting, heart rate increased, mean arterial pressure and total peripheral resistance were higher and decreased steeply after an initial increase. Discussion Migraineurs who developed a migraine-like attack in response to nitroglycerin showed stronger systemic cardiovascular responses compared to non-headache controls. The stronger systemic cardiovascular responses in migraine suggest increased systemic sensitivity to vasodilators, possibly due to insufficient autonomic compensatory mechanisms.


2002 ◽  
Vol 282 (5) ◽  
pp. R1459-R1467 ◽  
Author(s):  
T. D. Williams ◽  
J. B. Chambers ◽  
R. P. Henderson ◽  
M. E. Rashotte ◽  
J. M. Overton

We utilized variations in caloric availability and ambient temperature (Ta) to examine interrelationships between energy expenditure and cardiovascular function in mice. Male C57BL/6J mice ( n = 6) were implanted with telemetry devices and housed in metabolic chambers for measurement of mean arterial pressure (MAP), heart rate (HR), O2 consumption (V˙o 2), and locomotor activity. Fasting (Ta = 23°C), initiated at the onset of the dark phase, resulted in large and transient depressions in MAP, HR, V˙o 2, and locomotor activity that occurred during hours 6–17, which suggests torporlike episodes. Food restriction (14 days, 60% of baseline intake) at Ta = 23°C resulted in progressive reductions in MAP and HR across days that were coupled with an increasing occurrence of episodic torporlike reductions in HR (<300 beats/min) and V˙o 2 (<1.0 ml/min). Exposure to thermoneutrality (Ta = 30°C, n = 6) reduced baseline light-period MAP (−14 ± 2 mmHg) and HR (−184 ± 12 beats/min). Caloric restriction at thermoneutrality produced further reductions in MAP and HR, but indications of torporlike episodes were absent. The results reveal that mice exhibit robust cardiovascular responses to both acute and chronic negative energy balance. Furthermore, we conclude that Tais a very important consideration when assessing cardiovascular function in mice.


1994 ◽  
Vol 152 (2 Part 1) ◽  
pp. 554-561 ◽  
Author(s):  
A. Liu ◽  
C. Flores ◽  
T. Kinkead ◽  
A.A. Carboni ◽  
M. Menon ◽  
...  

1999 ◽  
Vol 87 (6) ◽  
pp. 2122-2127 ◽  
Author(s):  
Peter Lindholm ◽  
Patrik Sundblad ◽  
Dag Linnarsson

We sought to determine whether apnea-induced cardiovascular responses resulted in a biologically significant temporary O2 conservation during exercise. Nine healthy men performing steady-state leg exercise carried out repeated apnea (A) and rebreathing (R) maneuvers starting with residual volume +3.5 liters of air. Heart rate (HR), mean arterial pressure (MAP), and arterial O2 saturation (SaO2 ; pulse oximetry) were recorded continuously. Responses (ΔHR, ΔMAP) were determined as differences between HR and MAP at baseline before the maneuver and the average of values recorded between 25 and 30 s into each maneuver. The rate of O2 desaturation (ΔSaO2 /Δ t) was determined during the same time interval. During apnea, ΔSaO2/Δ t had a significant negative correlation to the amplitudes of ΔHR and ΔMAP ( r 2 = 0.88, P < 0.001); i.e., individuals with the most prominent cardiovascular responses had the slowest ΔSaO2 /Δ t. ΔHR and ΔMAP were much larger during A (−44 ± 8 beats/min, +49 ± 4 mmHg, respectively) than during R maneuver (+3 ± 3 beats/min, +30 ± 5 mmHg, respectively). ΔSaO2 /Δ t during A and R maneuvers was −1.1 ± 0.1 and −2.2 ± 0.2% units/s, respectively, and nadir SaO2 values were 58 ± 4 and 42 ± 3% units, respectively. We conclude that bradycardia and hypertension during apnea are associated with a significant temporary O2 conservation and that respiratory arrest, rather than the associated hypoxia, is essential for these responses.


1992 ◽  
Vol 20 (2) ◽  
pp. 121-126
Author(s):  
K Mikawa ◽  
N Maekawa ◽  
R Goto ◽  
H Yaku ◽  
N Saitoh ◽  
...  

The efficacy of intravenous mexiletine in attenuating the cardiovascular responses to laryngoscopy and tracheal intubation was studied in 30 normotensive patients undergoing elective surgery. The patients were randomly allocated to one of three treatment groups: saline ( n = 10); 2 mg/kg mexiletine ( n = 10); and 3 mg/kg mexiletine ( n = 10). The placebo/mexiletine was administered immediately before induction of anaesthesia using 5 mg/kg thiopentone and tracheal intubation was facilitated with 0.2 mg/kg vecuronium; laryngoscopy lasting 30 s was attempted 2 min after induction of anaesthesia. All groups showed a significant ( P < 0.05) increase in mean arterial pressure and heart rate associated with tracheal intubation. The increase in mean arterial pressure was significantly ( P < 0.05) smaller in patients receiving 3 mg/kg mexiletine compared with those receiving either saline or 2 mg/kg mexiletine. There was no significant attenuation in heart rate in either of the mexiletine treatment groups compared with the saline group. It is concluded that 3 mg/kg mexiletine given intravenously provides a simple and effective method for attenuating the pressor response to laryngoscopy and tracheal intubation.


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