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Hotel Sunrise is 300 m from the beach in the coastal resort of Ravda. It offers air-conditioned rooms with a balcony. Nessebar and Sunny Beach are less than 6 km away. Rooms here are fitted with a cable TV and refrigerator. Some also have a well-equipped kitchen. The balconies include garden furniture and Wi-Fi is free in all rooms.
National and international dishes are served at the restaurant. Guests can also dine on the ivy-covered terrace, which faces the street.
Ravda’s main street is only 100 m away and is lined up with restaurants and shops. The bus line to Nessebar and Sunny Beach stops only 200 m from Sunrise Hotel. Burgas Airport is 20 km away. Children and extra beds Free!
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One child under 5 years stays free of charge when using existing beds. One child under 5 years stays free of charge in an extra bed.
One older child or adult is charged BGN 9.78 per person per night in an extra bed. The maximum number of extra beds in a room is 1. Any type of extra bed or child's cot/crib is upon request and needs to be confirmed by management. Supplements are not calculated automatically in the total costs and will have to be paid for separately during your stay.
Natriuretic regulation of extracellular fluid volume homeostasis includes suppression of the renin-angiotensin-aldosterone system, pressure natriuresis, and reduced renal nerve activity, actions that concomitantly increase urinary Na + excretion and lead to increased urine volume. The resulting natriuresis-driven diuretic water loss is assumed to control the extracellular volume. Here, we have demonstrated that urine concentration, and therefore regulation of water conservation, is an important control system for urine formation and extracellular volume homeostasis in mice and humans across various levels of salt intake. We observed that the renal concentration mechanism couples natriuresis with correspondent renal water reabsorption, limits natriuretic osmotic diuresis, and results in concurrent extracellular volume conservation and concentration of salt excreted into urine.
This water-conserving mechanism of dietary salt excretion relies on urea transporter–driven urea recycling by the kidneys and on urea production by liver and skeletal muscle. The energy-intense nature of hepatic and extrahepatic urea osmolyte production for renal water conservation requires reprioritization of energy and substrate metabolism in liver and skeletal muscle, resulting in hepatic ketogenesis and glucocorticoid-driven muscle catabolism, which are prevented by increasing food intake.
This natriuretic-ureotelic, water-conserving principle relies on metabolism-driven extracellular volume control and is regulated by concerted liver, muscle, and renal actions. It has long been viewed that the maintenance of osmotic balance in response to high salt intake is a passive process that is mediated largely by increased water consumption to balance the salt load. Two studies in this issue of the JCI challenge this notion and demonstrate that osmotic balance in response to high salt intake involves a complex regulatory process that is influenced by hormone fluctuation, metabolism, food consumption, water intake, and renal salt and water excretion.