Heart atria

I] (pyr1)apelin-13 used to characterise native apelin receptors in human heart (atria and ventricles) bound with a single high affinity ( AD = 0.4 nM),... 

Describe the functions of the three major mechanical components of the heart atria, ventricles, and valves... 

Several lines of evidence suggest that tt2A- and a2c-receptors operate also in wild-type mice as integral parts of the presynaptic feedback loop. Experiments on peripheral tissues, e.g. heart atria, demonstrated that the a2c-subtype mediates autoinhibition by low concentrations of noradrenaline in wild-type mice, whereas the potency of noradrenaline at the a2A-subtype was lower (Fig. 4) (Hein et al. 1999). This potency difference of noradrenaline for the a2-receptors correlated with the affinity difference of noradrenaline for the tt2A- and a2c-subtypes, respectively. Furthermore, there is no evidence so far that the expression of the remaining o(2-receptor subtypes was altered in mice carrying deletions in a2A- or a2c-receptor genes (Link et al. 1995 Altman et al. 1999). 

Fig. 3 Autoreceptor versus heteroreceptor functions of a2-adrenoceptor subtypes, (a and b) Inhibition of electrically evoked [3H]-adrenaline release by the 012-agonist, medetomidine, from mouse brain cortex (a) or heart atria (b). In wild-type tissue specimens, medetomidine inhibited transmitter release by >90%. In tissues from a2AC-deficient mice, the agonist effect was absent (a, cortex) or significantly reduced (b, atria). Reproduced with permission from Trendelenburg et al. 2003b. (c) Overview of auto- and heteroreceptor functions of a2-adrenoceptor subtypes. For references, see text.

Effects of inhibitory receptors on K+ channels in tissues other than heart atria... 

Cohen SA 1996 Immunocytochemical localization of rHl sodium channel in adult rat heart atria and ventricle. Presence in terminal intercalated disks. Circulation 94 3083-3086... 

FIGURE 25 Atrial natriuretic factor (ANF) is a polypeptide hormone fliat is secreted mainly by flie heart atria in response to increases in atrial pressure or atrial stretch. 

Increased heart rate in response to leukotrienes is an autonomic reflex mediated by (3-adrenoceptors. The increase in heart rate was antagonized by the p-antagonist propranolol in both marine toads [36] and warm-acclimated bullfrogs [9]. The lack of reflex response to leukotrienes in cold-acclimated frogs suggested that P-adrenoceptor number may decrease during cold exposure. Heart atria and... 

Schlosser B, Kudernatsch MB, Sutor B et al (1995) Delta, mu and kappa opioid receptor agonists inhibit dopamine overflow in rat neostriatal slices. Neurosci Lett 191 126-30 Schwertfeger E, Klein T, Vonend O et al (2004) Neuropeptide Y inhibits acetylcholine release in human heart atrium by activation of Y2-receptors. Naunyn-Schmiedeberg s Arch Pharmacol... 

HEART- 2DPAGE German Heart Institute, Berlin Human heart (ventricle) Human heart (atrium) http //userpage.chemie.fu-berlin.de/ pldss/dhzb.html Pleissner et al., 1996... 

LimbergerN, Trendelenburg AU, Starke K. Pharmacological characterization of presynaptic a2-autoreceptors in rat submax illary gland and heart atrium. BrJ Pharmacol 1992 107 246-255. 

Noradrenaline Rat Vas deferens, heart atrium Electrically evoked H]noradrenaline release Ishac etal. 1996... 

DPAGE Institute, Berlin berlin.de/ pleiss/dhzb.html (ventricle) Human heart (atrium)... 

In rat brain the 5-HT4L-R is detectable throughout the brain, except in the cerebellum. The 5-HT4S-R is restricted to the striatum. Both isoforms are also present in peripheral tissues such as ileum, colon and bladder. The heart atrium expresses only 5-HTg-Rs. 

Pacing leads can be subdivided into a number of groups based on the area of placement and method of stimolation. Leads can be placed either on the epicardium (external surface) of the heart or, by a transvenous route, onto the endocardium (internal surface) of the right heart atrium or ventricle. Epicardial leads are used for permanent pacing in pediatric cases, where size considerations or congmtal defects prevent transvenous placement, and in patients who have undergone tricuspid valve rqilacement (Mitrani et al., 1999). Transvenous placement of the lead is the preferred route in most patients. 

Nontraditional Hormones. Novel hormones identified ia cardiovascular tissue have profound effects on maintenance of blood pressure and blood volume ia mammals. Atrial natriuretic hormone (ANH) is a polypeptide hormone secreted from the atria of the heart. When the cardiac atrium is stretched by increased blood volume, secretion of ANH is stimulated ANH ia turn increases salt and water excretion and reduces blood pressure (6). Endothelin is a polypeptide hormone secreted by endothehal cells throughout the vasculature. Although endothelin is released into the circulation, it acts locally in a paracrine fashion to constrict adjacent vascular smooth muscle and increase blood pressure (7). 

Transesophageal echocardiogram A procedure used to generate an image of the heart using sound waves, via a probe introduced into the esophagus (rather than the traditional transthoracic view) in order to obtain a better image of the left atrium. 

The atria (sing, atrium) are chambers that receive blood returning to the heart through the veins. The blood then moves to the ventricles, or delivery chambers, of the heart. The powerful contractions of the ventricles generate a force... 

The sinoatrial (SA) node is located in the wall of the right atrium near the entrance of the superior vena cava. The specialized cells of the SA node spontaneously depolarize to threshold and generate 70 to 75 heart beats/ min. The "resting" membrane potential, or pacemaker potential, is different from that of neurons, which were discussed in Chapter 3 (Membrane Potential). First of all, this potential is approximately -55 mV, which is less negative than that found in neurons (-70 mV see Figure 13.2, panel A). Second, pacemaker potential is unstable and slowly depolarizes toward threshold (phase 4). Two important ion currents contribute to this slow depolarization. These cells are inherently leaky to sodium. The resulting influx of Na+ ions occurs through channels that differ from the fast Na+ channels that cause rapid depolarization in other types of excitable cells. Toward the end of phase... 

From the SA node, the heart beat spreads rapidly throughout both atria by way of the gap junctions. As mentioned previously, the atria are stimulated to contract simultaneously. An interatrial conduction pathway extends from the SA node to the left atrium. Its function is to facilitate conduction of the impulse through the left atrium, creating the atrial syncytium (see Figure 13.3). 

Figure 13.3 Route of excitation and conduction in the heart. The heart beat is initiated in the sinoatrial (SA) node, or the pacemaker, in the right atrium of the heart. The electrical impulse is transmitted to the left atrium through the interatrial conduction pathway and to the atrioventricular (AV) node through the intemodal pathway. From the AV node, the electrical impulse enters the ventricles and is conducted through the AV bundle, the left and right bundle branches, and, finally, the Purkinje fibers, which terminate on the true cardiac muscle cells of the ventricles.

In addition to serving as blood reservoirs, veins help to regulate cardiac output (CO) by way of changes in venous return (VR). Venous return is defined as the volume of blood that flows from the systemic veins into the right atrium per minute. As discussed in Chapter 14 (cardiac output), a healthy heart pumps all of the blood returned to it. Therefore, CO is equal to VR ... 

HT4 receptors are also present in the pig and human hearts, primarily located in the atrium [9]. Experiments showed that stimulation of these receptors can result in tachycardia and can trigger positive inotropic effects. Moreover, it has been demonstrated that the 5-HT4 receptor is present in the human detrusor muscle and facilitates a cholinergic mechanism which may lead to increased bladder contractions [10]. Finally, acute (but not repeated) stimulation of 5-HT4 receptors present on the human adrenal cortex has been reported to trigger the release of corticosterone and aldosterone [11]. 

Elementary students are taught to think of the heart as a pump built according to a single straightforward pattern any variations from the pattern which might exist would be trifling, except, of course, in "abnormal" cases. That such is far from the case is shown by the twelve variations in the right atrium of the heart (Fig. 8). The forms of the valves of the inferior vena cava vary so much and the detailed structures are so different in size and contour as to make one almost doubt that the hearts are from the same species. 

The a wave This is caused by atrial contraction and is, therefore, seen before the carotid pulsation. It is absent in atrial fibrillation and abnormally large if the atrium is hypertrophied, for example with tricuspid stenosis. Cannon waves caused by atrial contraction against a closed tricuspid valve would also occur at this point. If such waves are regular they reflect a nodal rhythm, and if irregular they are caused by complete heart block. 

The x descent The fall at x is caused by downward movement of the heart during ventricular systole and relaxation of the atrium. 

Chronotropism and inotropism Isolated atrium/papillary muscle/ isolated hearts Sugiyama et al.,-86 Voss et al.87... 

Atrial natriuretic factor (ANF), produced by cells in the atrium of the heart in response to distension, binds the ANF receptor in vascular smooth muscle and in the kidney. The ANF receptor spans the membrane and has guanylate cyclase activity associated wMi the cytoplasmic domain. It causes relaxation of vascular smooth muscle, resulting in vasodilation, and in the kidney it promotes sodium and water excretion. 

Depolarisation of the membrane of the cardiomyocyte, resulting from the action potential, initiates contraction in cardiac as in skeletal muscle. This depolarisation arises in the sinoatrial node, a small group of cells in the right atrium, and then spreads through the heart causing, first, the muscles in the atria to contract and then the muscles in the ventricles to contract. 

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