Cognitive, or executive, control refers to the ability to coordinate thought and action and direct it toward obtaining goals. Evidence suggests that structures in the frontal lobe, particularly the prefrontal cortex (PFC), are critical for executive control. Here we review the role of the PFC. Perhaps most importantly, the PFC transmits acquired knowledge. Its neural activity reflects learned task contingencies, concepts, and rules. In short, the PFC seems to underlie our internal representations of the ‘rules of the game’. This may provide the foundation for the complex behavior of primates, in whom this structure is most elaborate.

Executive Function and Higher-Order Cognition: Definition and Neural Substrates

RhoA/Rho-kinase pathway plays an important role in many pathological conditions. RhoA participates in the regulation of smooth muscle tone and activates many downstream kinases. The best characterized are the serine/threonine kinase isoforms (Rho-kinase or ROCK), ROCKα/ROCK2 and ROCKβ/ROCK1. ROCK is necessary for diverse functions such as local blood flow, arterial/pulmonary blood pressure, airway resistance and intestinal peristalsis. ROCK activation permits actin/myosin interactions and smooth muscle cells contraction by maintaining the activity of myosin light-chain kinase, independently of the free cytosolic calcium level. The sensitization of smooth muscle myofilaments to calcium has been implicated in many pathological states, such as hypertension, diabetes, heart attack, stroke, pulmonary hypertension, erectile dysfunction, and cancer. The focus of this review is on the involvement of RhoA/Rho-kinase in diseases. We will briefly describe the ROCK isoforms and the role of RhoA/Rho-kinase in the vasculature, before exploring the most recent findings regarding this pathway and various diseases.

/pdf/rhoa-rho-kinase-and-vascular-diseases-what-is-the-link-4gf5f1rovw.pdf

RhoA/Rho-kinase and vascular diseases: what is the link?

The emerging critical implications of Rho/Rho-kinase (ROCK) signaling in neurodegenerative diseases, glaucoma, renoprotection, diabetes and cancer have sparked growing interest in the pharmacological potential of ROCK inhibitors beyond their current application in cardiovascular disease. This article discusses the therapeutic benefits of novel ROCK inhibitors in development, and highlights the recent advances in the current understanding of disease-dependent and isoform-specific functions of ROCK and their potential impact on future therapeutic strategies.

Rho-kinase inhibitors as therapeutics: from pan inhibition to isoform selectivity

The Endothelial–Erectile Dysfunction Connection: An Essential Update

Endothelial nitric oxide (NO) synthase (eNOS) has an indispensable role in the erectile response. In the penis, eNOS activity and endothelial NO bioavailability are regulated by multiple post-translational molecular mechanisms, such as eNOS phosphorylation, eNOS interaction with regulatory proteins and contractile pathways, and actions of reactive oxygen species (ROS). These mechanisms regulate eNOS-mediated responses under physiologic circumstances and provide various mechanisms whereby endothelial NO availability may be altered in states of vasculogenic erectile dysfunction (ED). In view of the recent advances in the field of eNOS function in the penis and its role in penile erection, the emphasis in this review is placed on the mechanisms regulating eNOS activity and its interaction with the RhoA/Rho-kinase pathway in the physiology of penile erection and the pathophysiology of ED.

eNOS Function and Dysfunction in the Penis

Physiological aging is a significant risk factor in the on-set of male erectile dysfunction (ED) and an imbalance in factors that modulate cavernosal smooth-muscle tone may play a role in these altered penile hemodynamic mechanisms. To evaluate the association between aging and male erectile function, we monitored neurogenic erectile response and its correlation to systemic arterial pressure changes in old (21-23 months of age) vs young (6-9 months of age) Brown-Norway (BN) rats. We tested the hypothesis that age-associated ED is due to unregulated vasoconstrictive tone, contributed in part by an increased Rho-kinase activity, and that antagonism of Rho-kinase activity attenuates the age-related decline in male erectile function. We also examined the hypothesis that a combination of Rho-kinase antagonism and phosphodiesterase-5 (PDE-5) inhibition has a synergistic effect in improving the erectile response in these aging animals. Erectile function in old BN rats was evaluated before and after intracavernosal injection of a specific inhibitor of Rho-kinase (Y-27632) alone or in combination with zaprinast, a PDE-5 inhibitor. Erectile capabilities of the young and old BN rat groups were significantly different in corpus cavernosum pressure response after electrical-field stimulation of the major pelvic ganglion. Y-27632 administration attenuated the aging-related changes in male erectile function seen in BN rats. Rho-kinase antagonism and PDE-5 inhibition had a synergistic effect in improving erectile function in old rats. Our data indicate that aging leads to impairment in the neurogenic erectile response in BN rats involving a possible derangement in penile hemodynamic mechanisms of the erectile tissue. Rho-kinase inhibition may be of value in treating age-related ED.

Rho-kinase inhibition improves erectile function in aging male Brown-Norway rats.

Rho-Kinase Inhibition Suppresses Potassium Chloride-Induced Bladder Hyperactivity in a Rat Model

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Rho-kinase inhibition improves erectile function in aging male Brown-Norway rats.

Rho-Kinase Inhibition Suppresses Potassium Chloride-Induced Bladder Hyperactivity in a Rat Model