Other factors and research
Regular difficulty reaching orgasm after ample sexual stimulation, known as anorgasmia, is significantly more common in women than in men (see below). In addition to sexual dysfunction being a cause for womens inability to reach orgasm, or the amount of time for sexual arousal needed to reach orgasm being variable and longer in women than in men, other factors include a lack of communication between sexual partners about what is needed for the woman to reach orgasm, feelings of sexual inadequacy in either partner, a focus on only penetration (vaginal or otherwise), and men generalizing womens trigger for orgasm based on their own sexual experiences with other women.Scholars state "many couples are locked into the idea that orgasms should be achieved only through intercourse [vaginal sex]" and that "[e]ven the word foreplay suggests that any other form of sexual stimulation is merely preparation for the main event.... ...Because women reach orgasm through intercourse less consistently than men, they are more likely than men to have faked an orgasm". Sex counselor Ian Kerner stated, "Its a myth that using the penis is the main way to pleasure a woman." He cites research concluding that women reach orgasm about 25% of the time with intercourse, compared with 81% of the time during oral sex (cunnilingus).In the first large-scale empirical study worldwide to link specific practices with orgasm, reported in the Journal of Sex Research in 2006, demographic and sexual history variables were comparatively weakly associated with orgasm.
Beta blockers, in addition to their sympatholytic β1 activity in the heart, influence the renin–angiotensin system at the kidneys. Beta blockers cause a decrease in renin secretion, which in turn reduces the heart oxygen demand by lowering the extracellular volume and increasing the oxygen-carrying capacity of the blood. Heart failure characteristically involves increased catecholamine activity on the heart, which is responsible for several deleterious effects, including increased oxygen demand, propagation of inflammatory mediators, and abnormal cardiac tissue remodeling, all of which decrease the efficiency of cardiac contraction and contribute to the low ejection fraction. Beta blockers counter this inappropriately high sympathetic activity, eventually leading to an improved ejection fraction, despite an initial reduction in ejection fraction. Trials have shown beta blockers reduce the absolute risk of death by 4.5% over a 13-month period. In addition to reducing the risk of mortality, the numbers of hospital visits and hospitalizations were also reduced in the trials.Therapeutic administration of beta blockers for congestive heart failure ought to begin at very low doses (1/8 of target) with a gradual escalation of the dose. The heart of the patient must adjust to decreasing stimulation by catecholamines and find a new equilibrium at a lower adrenergic drive. Anxiety
Officially, beta blockers are not approved for anxiolytic use by the U.S. Food and Drug Administration. However, many controlled trials in the past 25 years indicate beta blockers are effective in anxiety disorders, though the mechanism of action is not known.